Structure-function relationship

● Dissociation Logic in Lesion Studies

Dissociation logic in lesion studies is used to understand which brain areas are essential
for specific cognitive or behavioral functions by examining the effects of damage to
certain regions. Lesion studies in neuropsychology often involve patients with brain
injuries or animals with experimentally induced lesions. Researchers apply dissociation
logic to identify patterns in behavior or cognitive deficits resulting from these lesions. The
key concepts are single dissociation and double dissociation, each providing different
insights:
○ Single Dissociation:
This occurs when damage to a specific brain area affects one cognitive function
but leaves another intact. For example, if damage to a particular brain area
impairs memory but not language, it suggests that the affected region is crucial
for memory. However, a single dissociation does not conclusively prove that the
two functions are entirely separate—it could mean the task is simply more
demanding.
○ Double Dissociation:
To get a stronger conclusion, researchers look for a double dissociation, which
involves two separate brain lesions affecting two distinct functions independently.
For example, if damage to Area A affects memory but not language, and damage
to Area B affects language but not memory, this pattern provides stronger
evidence that memory and language rely on different neural structures. Double
dissociations are therefore more convincing in identifying independent cognitive
processes and linking them to specific brain regions.
● Together, these dissociation techniques are foundational in neuropsychology, helping
map the brain’s architecture and understanding how distinct areas contribute to different
functions.
● Different brain areas and their respective functions? Basic anatomy and physiology.
The human brain is a highly complex organ divided into different regions, each
responsible for various functions. Here’s a basic overview of key brain areas and their
respective functions:
1. Cerebrum
○ Location: Largest part, encompassing most of the brain’s mass
○ Functions: Responsible for higher cognitive functions, like reasoning,
problem-solving, emotion, and motor function.
○ Division:
■ Frontal Lobe: Controls voluntary movements, decision-making,
problem-solving, social behaviour and understanding, personality, and
emotions.
■ Patients with ADHD, anxiety or depression have less control of the
prefrontal cortex (less developed)
 ■ Parietal Lobe: Processes sensory information like touch, temperature,
and pain and helps with spatial orientation.
■ Occipital Lobe: Manages visual processing.
■ Temporal Lobe: Involved in memory, language comprehension, and
processing auditory information.
● 2. Cerebellum
○ Location: Below the occipital lobe at the brain's base
○ Functions: Coordinates fine motor skills, balance, and posture. It helps make
movements smooth and is critical for activities that require precision.
● 3. Brainstem
○ Location: Connects the brain to the spinal cord
○ Functions: Controls automatic, vital functions, like heart rate, breathing, and
digestion. It also plays a role in sleep-wake cycles.
○ Subsections:
■ Midbrain: Involved in visual and auditory reflexes and eye movement.
■ Pons: Assists in regulating breathing and relays messages between the
cerebrum and cerebellum.
■ Medulla Oblongata: Manages involuntary functions like breathing, blood
pressure, and heart rate.
● 4. Limbic System
○ Location: Deep within the brain
○ Functions: Manages emotions, memories, and arousal. It's often called the
“emotional brain.”
○ Key Parts:
■ Amygdala: Processes emotions, particularly fear and pleasure.
■ Hippocampus: Essential for forming new memories and spatial
navigation.
■ Thalamus: Acts as a relay station, channeling sensory information to the
appropriate cortical areas.
■ Hypothalamus: Regulates hormones, hunger, thirst, and body
temperature and links the nervous system to the endocrine system.
● 5. Basal Ganglia
○ Location: Deep within the cerebral hemispheres
○ Functions: Plays a role in motor control, procedural learning, and routine
behaviors or “habits.” It's involved in voluntary motor movements and is key in
conditions like Parkinson’s disease.
● 6. Corpus Callosum
○ Location: Central area connecting the two hemispheres of the brain
○ Functions: Facilitates communication between the left and right hemispheres of
the brain.
● Explanations, cause and effect of the mentioned cases?
Gage: damage to the prefrontal cortex, resulting in a change of personality, rude,
 Louis Victor Leborgne, also “Tan”: Brocca’s Aphasia, decline in production of speech as
well as reading and writing
● How can we study cognitive functions? How can we study relationship within the brain?
(experiments, studies, medical approaches)
■ Neuroimaging Techniques
■ Functional Magnetic Resonance Imaging (fMRI): Measures blood flow
changes associated with brain activity, showing which areas are active
during specific cognitive tasks. Used for studying memory, attention,
decision-making, and more.
■ Electroencephalography (EEG): Records electrical activity via scalp
electrodes to study brain waves. EEG is particularly effective for
understanding timing in cognitive processes like attention and reaction to
stimuli.
■ Positron Emission Tomography (PET): Involves injecting a radioactive
tracer to visualize metabolic activity in the brain. It’s useful in mapping
cognitive functions and diagnosing conditions like Alzheimer’s.
■ Magnetoencephalography (MEG): Detects magnetic fields produced by
neural activity, combining temporal resolution like EEG with better spatial
resolution. MEG helps pinpoint areas involved in language, memory, and
sensory processing.
■ Lesion Studies
■ Studying people with specific brain damage (e.g., stroke or traumatic
brain injury) reveals how the loss of certain brain regions impacts
cognition. For example, research on patients with damage to the
hippocampus has been crucial for understanding memory processes.
■ Transcranial Magnetic Stimulation (TMS)
■ Description: Uses magnetic fields to stimulate specific brain regions
temporarily, allowing researchers to “turn off” an area momentarily and
observe changes in behavior or cognitive function.
■ Purpose: This method helps to infer causation, showing how suppressing
specific brain areas impacts abilities like motor control or language
processing.
■ Cognitive and Behavioral Testing
■ Neuropsychological Assessments: Standardized tests (e.g., the Stroop
test, the Wisconsin Card Sorting Test) measure attention, memory,
problem-solving, and executive functions.
■ Behavioral Experiments: Often combined with neuroimaging, these
studies present tasks or puzzles to examine how the brain handles
cognitive load, decision-making, memory recall, and perception.
■ Single-Cell Recording (Invasive)
■ Primarily used in animal studies, electrodes record the activity of
individual neurons, showing how they respond to stimuli or tasks. In
humans, this method is typically restricted to individuals undergoing
 surgery for epilepsy or other conditions where electrodes are already in
place.
■ Genetic and Pharmacological Studies
■ Genetics: Understanding how genes impact brain structure and function
(e.g., twin studies, genome-wide association studies) provides insight into
heritable cognitive traits and susceptibility to cognitive disorders.
■ Pharmacology: Studying the effects of specific drugs on cognition
reveals the role of neurotransmitters. For example, dopamine’s role in
reward and motivation can be studied by administering drugs that
enhance or block dopamine.
■ Longitudinal Studies
■ In these studies, researchers follow the same participants over an
extended period to observe changes in cognitive functions, brain
structure, and behavior. Longitudinal research helps uncover how aging,
neurodevelopmental changes, or diseases like Alzheimer’s affect the
brain over time.
■ Machine Learning and Brain Connectivity Analysis
■ Techniques like connectomics map networks of interconnected brain
areas to understand how different regions communicate and work
together. By applying machine learning to brain imaging data, researchers
can predict how specific brain regions interact and may contribute to
cognitive functions.

● The Graph
○ Single dissociation interpretation
Single dissociation shows that Region A is crucial for Function X but not for
Function Y. However, it doesn’t clarify whether Function X and Function Y are
entirely independent processes.
○ Double dissociation interpretation
Double dissociation indicates that Region A is specifically responsible for
Function X, while Region B is specifically responsible for Function Y. This pattern
provides strong evidence that these functions are independent and rely on
distinct brain regions.

Neuropsychology, Cognitive Neuroscience

and Behavioral Brain Science
● Neuropsychology
Department Overview: The course is part of the Faculty of Psychology and
Neuroscience, focusing on neuropsychology and pharmacology. Research includes
Mobile Brain Void Imaging and the study of brain anatomy .
○ Cognitive Functions and Disorders
■ Cognitive Neuroscience: Focuses on brain functions related to
cognition, including memory, attention, and motor control .
■ Clinical Applications: Research includes studying disorders like
Alzheimer's and Parkinson's, exploring how music and timing can aid
recovery .
○ Research Methods
■ Mobile Brain Imaging: This method records brain activity while
participants perform tasks, using EMGs and 3D motion tracking .
■ Transcranial Magnetic Stimulation (TMS): A non-invasive technique to
manipulate brain activity, useful for both research and treatment of brain
disorders .
○ Neuroscience Techniques
■ Functional Imaging: Techniques like fMRI and TMS are used to study
brain structure and function, emphasizing the importance of methodology
in neuroscience .
■ Neuronal Communication: Neurons communicate via action potentials
and neurotransmitters, with a focus on how these processes relate to
cognitive functions .
○ Cognitive Tasks
■ Perception: Understanding how sensory information is processed, with a
focus on the visual system .
■ Attention: Exploring how we actively seek information and focus on
relevant stimuli .
■ Memory: Differentiating between short-term and long-term memory, and
their implications for learning .
○ Motor Control
■ Motor Neurons and Movement: The organization of motor control
circuits, including the role of the cerebellum in fine-tuning movements .
○ Neuromodulation and External Influences
■ Influence of Diet and Drugs: Examining how substances like tryptophan
affect serotonin levels and mood, alongside other factors like exercise
and psychedelics .
○ Assessment and Learning Approach
■ PBL Methodology: Students are encouraged to engage in self-directed
learning and research, utilizing various textbooks and resources .
■ Evaluation Philosophy: The course emphasizes continuous assessment
through midterm and final reviews, focusing on feedback and mastery of
content .
 ● Behavioral Brain Science
The lecture explores the relationship between the brain and behavior, emphasizing that
our understanding of the brain is still evolving. The speaker invites participants to
engage actively by writing down thoughts and questions throughout the session .
○ Frontiers in Science
The universe is expanding rapidly, and phenomena like black holes challenge our
understanding of mass and gravity . At the microscopic level, the brain's
functioning is another frontier that remains largely unexplored .
○ Hormonal Influences on Behavior
Hormones significantly influence behavior, as seen in various life events like
menstruation and stress responses . The speaker discusses how certain
behaviors can be linked to hormonal changes, which can even affect legal
outcomes in court cases .
○ Brain Function Myths
The myth that humans only use 10% of their brains is debunked. In reality, brain
imaging shows that all parts of the brain are active, and damage to any area can
have significant consequences .
○ Neurons and Connections
The brain consists of approximately 100 billion neurons, each forming numerous
connections, which are crucial for cognitive functions . The process of
neurogenesis and the formation of new connections is vital for learning and
memory .
○ Brain Anatomy
The human brain's structure includes the cortex, cerebellum, and brainstem,
each responsible for different functions. The cortex is involved in complex
processes, while the cerebellum coordinates movement .
○ Levels of Explanation in Brain Function
Understanding brain function requires examining multiple levels, from social
influences to neural systems and cellular mechanisms. For instance, oxytocin
can enhance social interactions but may also increase aggression towards
strangers .
○ Conclusion and Engagement
The lecture concludes with an interactive element, encouraging participants to
reflect on what they learned through a fun activity involving a song about brain
parts .

Neurons I

● The function of each part of a neuron

○ Dendrites
Dendrites are branch-like extensions that receive signals from other neurons and
convey this information to the cell body. They are specialized to detect chemical
signals from neighboring neurons and convert them into small electrical impulses.
○ Cell Body (Soma)
The cell body contains the nucleus and other organelles necessary for the cell’s
 survival and function. It integrates incoming signals from the dendrites and
determines if the signal is strong enough to be sent further.
○ Nucleus
Located within the cell body, the nucleus contains genetic material (DNA) and
regulates cell functions, including protein synthesis, which supports neuron
activity and maintenance.
○ Axon
The axon is a long, slender projection that carries electrical impulses away from
the cell body toward other neurons or effectors (muscles or glands). It’s the main
conducting unit of the neuron, allowing for long-distance signal transmission.
○ Myelin Sheath
The myelin sheath is a fatty layer that wraps around the axon, formed by glial
cells (Schwann cells in the peripheral nervous system and oligodendrocytes in
the central nervous system). It insulates the axon, speeding up the transmission
of electrical impulses along the neuron.
○ Nodes of Ranvier
These are gaps in the myelin sheath along the axon. The electrical impulse
“jumps” from one node to the next, in a process called saltatory conduction,
which increases the speed of transmission.
○ Axon Terminals (Terminal Buttons)
The axon terminals are the small, branching structures at the end of the axon that
release neurotransmitters. When an electrical impulse reaches the axon terminal,
it triggers the release of neurotransmitters into the synaptic cleft, which then bind
to receptors on the dendrites of a neighboring neuron, passing along the signal.
○ Synapse (Synaptic Cleft)
The synapse is the gap between the axon terminal of one neuron and the
dendrites of another. Neurotransmitters released into the synaptic cleft carry the
signal from one neuron to the next, allowing for communication between cells.

● What is the structure of a membrane (transportation)

○ Phospholipid Bilayer
■ Phospholipids: These molecules form the basic framework of the
membrane, arranged in two layers. Each phospholipid has a hydrophilic
(water-attracting) "head" and two hydrophobic (water-repelling) "tails."
■ Bilayer Formation: The hydrophilic heads face the aqueous environment
on the outside and inside of the cell, while the hydrophobic tails face each
other, forming a barrier that prevents many substances from freely
crossing the membrane.
■ Selective Permeability: Small, nonpolar molecules (like oxygen and
carbon dioxide) can pass directly through the bilayer, but polar or large
molecules require specific pathways.
 ○ Membrane Proteins
■ Integral Proteins: These span across the membrane and often act as
channels or carriers to facilitate the transport of specific ions or
molecules. They are critical for active and facilitated transport.
■ Peripheral Proteins: Located on the surface of the membrane, these are
involved in signaling and help support cell shape but typically don’t play a
direct role in transportation.
■ Transport Proteins: Specific integral proteins, such as channel proteins
and carrier proteins, allow substances that cannot directly pass through
the lipid bilayer to enter or exit the cell.
○ Cholesterol
■ Cholesterol molecules are interspersed within the phospholipid bilayer.
They help stabilize the membrane’s fluidity, making it less permeable to
very small water-soluble molecules that might otherwise pass freely.
■ Cholesterol also contributes to membrane integrity, especially in varying
temperature conditions, ensuring the membrane remains flexible but
intact.
○ Carbohydrate Chains
■ Attached to proteins (glycoproteins) or lipids (glycolipids) on the
extracellular surface of the membrane, these carbohydrate chains play a
role in cell recognition and communication.
■ They can help in identifying cells and are involved in the immune
response and cellular signaling, though they do not directly participate in
transport.
● Membrane Transportation Mechanisms
The structure of the cell membrane supports various transportation mechanisms:
○ Passive Transport: Does not require energy. It includes:
■ Diffusion: Movement of small, nonpolar molecules (e.g., O₂, CO₂) directly
through the bilayer.
■ Facilitated Diffusion: Movement of polar or large molecules through
channel or carrier proteins.
■ Osmosis: Diffusion of water through aquaporins, a type of channel
protein.
○ Active Transport: Requires energy (ATP) to move substances against their
concentration gradient.
■ Pumps: Transport proteins (like the sodium-potassium pump) actively
move ions across the membrane.
■ Endocytosis and Exocytosis: Processes that involve the membrane
engulfing or expelling large particles or bulk substances using vesicles.

●
● Process of an action potential
This process involves rapid changes in membrane potential and can be divided into
several stages: resting state, depolarization, repolarization, and hyperpolarization.
Here’s a step-by-step overview:
1. Resting State
○ The neuron is at rest, typically at a membrane potential of around 70 mV (inside
is more negative relative to outside).
○ Sodium (Na⁺) ions are concentrated outside the cell, while potassium (K⁺) ions
are concentrated inside.
○ Sodium-potassium pumps actively maintain this concentration gradient by
moving 3 Na⁺ out and 2 K⁺ in, keeping the inside negatively charged relative to
the outside.
● 2. Depolarization (Threshold Reached)
○ When a stimulus reaches a certain threshold (typically around -55 mV),
voltage-gated sodium (Na⁺) channels open, and Na⁺ ions rush into the cell due
to the concentration and electrical gradients.
○ This influx of positive ions causes the membrane potential to become less
negative and eventually positive (around +30 mV).
○ Depolarization propagates down the neuron, creating an action potential along
the axon.
● 3. Repolarization
○ Once the membrane potential reaches a peak (+30 mV), Na⁺ channels close,
and voltage-gated potassium (K⁺) channels open.
○ K⁺ ions flow out of the cell, moving down their concentration gradient, which
brings the membrane potential back toward a more negative value.
● 4. Hyperpolarization (Refractory Period)
○ The K⁺ channels remain open a bit longer than needed, causing an overshoot
where the membrane potential becomes more negative than the resting state
(below -70 mV).
○ This period is known as hyperpolarization and ensures that the neuron briefly
cannot initiate another action potential, creating a refractory period that
prevents the signal from traveling backward.
● 5. Return to Resting State
○ The K⁺ channels close, and the sodium-potassium pump restores the resting
membrane potential by moving Na⁺ ions out and K⁺ ions back in.
○ The neuron is now ready to fire another action potential if a new stimulus reaches
the threshold.
● Summary
The action potential process involves:
○ Rapid influx of Na⁺ ions (depolarization).
○ Outflow of K⁺ ions (repolarization).
○ Temporary hyperpolarization and then restoration to resting potential by the
sodium-potassium pump.
● This rapid cycle allows neurons to transmit signals quickly and efficiently, enabling
communication across the nervous system.

● Understanding the graph of the action potential

1. Resting State
○ At this stage, the neuron is at its resting membrane potential, which is around 70
mV.
○ The voltage-gated sodium (Na⁺) and potassium (K⁺) channels are closed.
○ The sodium-potassium pump actively maintains this resting state by pumping 3
Na⁺ ions out and 2 K⁺ ions in, keeping the inside of the neuron more negative.
● 2. Depolarization (Threshold Reached)
○ A stimulus causes the membrane potential to reach a threshold around 55 mV.
○ This opens voltage-gated Na⁺ channels, allowing Na⁺ ions to rush into the cell.
○ The influx of Na⁺ ions makes the inside of the cell more positive, quickly raising
the membrane potential toward +30 mV.
● 3. Peak of Action Potential
○ At the peak (around +30 mV), Na⁺ channels close, and K⁺ channels begin to
open.
○ This is the highest point of the action potential, where the cell is briefly more
positive inside than outside.
● 4. Repolarization
○ With K⁺ channels open, K⁺ ions exit the cell, moving down their concentration
gradient.
○ This outflow of positive ions brings the membrane potential back down toward a
negative value, restoring the cell's polarity.
● 5. Hyperpolarization (Afterpotential)
○ The K⁺ channels stay open a bit longer than needed, causing the membrane
potential to drop slightly below the resting potential (more negative than -70 mV).
○ This is called hyperpolarization or the afterpotential.
○ This phase prevents the neuron from immediately firing another action potential,
creating a refractory period.
● Return to Resting State
○ The K⁺ channels close, and the sodium-potassium pump restores the resting
membrane potential by moving Na⁺ ions out and K⁺ ions in.
○ The neuron is now back to its resting state and ready for another action potential
if a new stimulus reaches the threshold.
 ● Key Points on the Graph
○ The dotted line at -55 mV represents the threshold potential; a stimulus needs
to reach this level to trigger an action potential.
○ The peak is around +30 mV, representing maximum depolarization.
○ After the action potential, the graph shows a dip below the resting level,
indicating hyperpolarization.

Neurons II

● What are the stages of a synaptic transmission/transfer?

Synaptic transmission is the process by which one neuron communicates with another
neuron or an effector cell, like a muscle cell.
1. Action Potential Arrival
○ An electrical signal, or action potential, travels down the axon of the presynaptic
neuron to the synaptic terminal.
● 2. Calcium Ion Influx
○ When the action potential reaches the axon terminal, it triggers voltage-gated
calcium (Ca²⁺) channels to open.
○ Calcium ions flow into the neuron due to the high concentration of calcium
outside the cell compared to inside.
● 3. Vesicle Fusion and Neurotransmitter Release
○ The influx of Ca²⁺ causes synaptic vesicles (containing neurotransmitters) to
move toward and fuse with the presynaptic membrane.
○ Through a process called exocytosis, neurotransmitters are released into the
synaptic cleft (the small gap between the presynaptic and postsynaptic cells).
● 4. Neurotransmitter Binding to Receptors
○ Neurotransmitters diffuse across the synaptic cleft and bind to specific receptors
on the postsynaptic membrane.
○ The type of receptor the neurotransmitter binds to will determine the response in
the postsynaptic cell.
● 5. Postsynaptic Potential Creation
○ Binding of neurotransmitters to receptors triggers ion channels in the
postsynaptic membrane to open or close.
○ This results in an excitatory postsynaptic potential (EPSP) or inhibitory
postsynaptic potential (IPSP), depending on whether the ion flow causes
depolarization or hyperpolarization of the postsynaptic cell.
● 6. Signal Termination
○ To prevent continuous signaling, neurotransmitters must be removed from the
synaptic cleft. This can occur by:
■ Reuptake: The neurotransmitter is reabsorbed by the presynaptic cell.
■ Enzymatic Degradation: Enzymes break down neurotransmitters in the
synaptic cleft.
■ Diffusion: Neurotransmitters diffuse away from the synaptic cleft.
● 7. Inhibition of overstimulation through potassium channels
8. Return to Resting State
○ The presynaptic and postsynaptic cells return to their resting states, ready to
participate in the next synaptic transmission.
● What are the differences between glutamate and GABA (gamma aminobutyric acid)
Glutamate and GABA (gamma-aminobutyric acid) are two of the most important
neurotransmitters in the brain and central nervous system (CNS).
1. Function and Type of Neurotransmitter
○ Glutamate: Excitatory neurotransmitter. It increases the likelihood of the
postsynaptic neuron firing an action potential. It plays a major role in excitatory
signaling and is crucial for learning, memory, and neuroplasticity.
○ GABA: Inhibitory neurotransmitter. It decreases the likelihood of the
postsynaptic neuron firing an action potential. GABA is essential for calming
neural activity and preventing overstimulation.
● 2. Receptors
○ Glutamate: Binds to multiple types of receptors, primarily NMDA, AMPA, and
kainate receptors. These receptors allow positive ions (such as calcium and
sodium) to enter the postsynaptic neuron, leading to depolarization and
increased excitatory signaling.
○ GABA: Binds to GABA_A and GABA_B receptors. GABA_A receptors are
ionotropic, allowing chloride ions to flow into the postsynaptic cell, causing
hyperpolarization. GABA_B receptors are metabotropic, which indirectly causes
hyperpolarization by modulating potassium channels.
● 3. Role in the Brain
○ Glutamate: Prominent in regions associated with cognitive functions such as the
cortex and hippocampus. It facilitates processes that require high brain activity,
including learning and memory formation.
○ GABA: Primarily involved in inhibiting brain activity, helping to maintain a balance
with glutamate. It has a calming effect on the brain and is involved in regulating
mood, anxiety, and sleep.
● 4. Synthesis and Precursors
○ Glutamate: Synthesized from glucose or other precursors in the brain and can
be formed from the amino acid glutamine.
○ GABA: Synthesized from glutamate itself through the enzyme glutamic acid
decarboxylase (GAD).
● 5. Effects of Imbalance
○ Glutamate: High levels or overactivity can lead to excitotoxicity, which can
damage neurons due to overstimulation. This is associated with
neurodegenerative diseases such as Alzheimer’s, Huntington’s, and multiple
sclerosis.
○ GABA: Low levels or underactivity can lead to heightened neural activity, which
may result in anxiety, epilepsy, and insomnia. Some medications (like
 benzodiazepines) enhance GABAergic activity to reduce anxiety and prevent
seizures.
● 6. Drug Interaction
○ Glutamate: Drugs that affect glutamate signaling include some anesthetics,
NMDA receptor antagonists, and certain antidepressants targeting excitatory
balance.
○ GABA: Drugs that increase GABA activity include benzodiazepines, barbiturates,
and certain anticonvulsants. These are often used to reduce anxiety, promote
relaxation, and prevent seizures.
● 7. Distribution in the CNS
○ Glutamate: Abundant throughout the CNS; almost every neuron in the brain can
be affected by glutamate.
○ GABA: Also widespread but particularly concentrated in areas involved in
inhibitory control and calming of excitatory signals.
● In summary, glutamate excites the brain and supports learning and memory, while
GABA calms the brain, preventing overstimulation and aiding in mood and sleep
regulation. Together, they maintain a balance that is essential for healthy brain function
and stable mental states.
● What other types of neurotransmitters exist?
Neurotransmitters come in several types, each with distinct roles in the body and brain.
1. Amino Acid Neurotransmitters
○ Glutamate: Primary excitatory neurotransmitter involved in memory and learning.
○ GABA (Gamma-Aminobutyric Acid): Primary inhibitory neurotransmitter that
calms neural activity.
○ Glycine: Another inhibitory neurotransmitter, mostly found in the spinal cord,
brainstem, and retina. It modulates motor and sensory pathways.
● 2. Monoamine Neurotransmitters
These are involved in regulating emotions, arousal, and cognition.
○ Dopamine: Plays roles in reward, motivation, and motor control. Imbalances are
associated with disorders like Parkinson's and schizophrenia.
○ Serotonin: Regulates mood, sleep, appetite, and digestion. It’s often targeted by
antidepressant medications to alleviate depression and anxiety.
○ Norepinephrine (Noradrenaline): Involved in arousal, alertness, and the
fight-or-flight response. It helps focus attention and is also implicated in mood
regulation.
○ Epinephrine (Adrenaline): Primarily a hormone but also acts as a
neurotransmitter in the brain to regulate the fight-or-flight response, increasing
heart rate and blood flow.
● 3. Peptide Neurotransmitters
Peptides are longer chains of amino acids and often serve dual roles as
neurotransmitters and hormones.
○ Endorphins: Natural painkillers that create feelings of euphoria and pain relief;
they're involved in exercise, excitement, and well-being.
 ○ Substance P: Involved in pain perception and the stress response.
○ Oxytocin: Known as the "love hormone," it plays a role in social bonding, trust,
and childbirth.
● 4. Purine Neurotransmitters
These include nucleotides and nucleosides involved in energy transfer, like ATP.
○ Adenosine: Generally inhibitory and plays a role in promoting sleep and
reducing arousal. Caffeine blocks adenosine receptors, leading to increased
alertness.
○ ATP (Adenosine Triphosphate): Often released along with other
neurotransmitters and involved in energy signaling and pain perception.
● 5. Acetylcholine (ACh)
○ Acetylcholine is critical for muscle contraction and is the primary neurotransmitter
at neuromuscular junctions.
○ In the brain, it’s involved in attention, learning, and memory. Acetylcholine deficits
are associated with Alzheimer’s disease.
● 6. Gasotransmitters
These are gaseous neurotransmitters, unique in that they diffuse through membranes
rather than binding to receptors.
○ Nitric Oxide (NO): Plays roles in vasodilation, learning, and memory by
modulating blood flow and neural communication.
○ Carbon Monoxide (CO): Although toxic at high levels, in small quantities it has
signaling roles in the brain, particularly related to inflammation and vasodilation.
● 7. Lipid-Based Neurotransmitters
These are derived from lipids and often work through retrograde signaling (sending
signals from the postsynaptic to the presynaptic neuron).
○ Endocannabinoids (e.g., Anandamide): Involved in mood, appetite, pain
sensation, and memory. They act on cannabinoid receptors and are mimicked by
compounds in cannabis.
● These different types of neurotransmitters collectively help regulate a wide range of
bodily functions, from movement and sensory perception to complex processes like
emotion, memory, and response to stress.
● What causes the chemical imbalance within depression?
The concept of a “chemical imbalance” in depression has been widely discussed, though
depression is now understood to involve a complex interplay of multiple factors beyond
just neurotransmitter levels.
1. Neurotransmitter Dysregulation
○ Serotonin: Low levels or impaired functioning of serotonin are strongly linked to
depression. Serotonin helps regulate mood, anxiety, and sleep. Antidepressants
like SSRIs (selective serotonin reuptake inhibitors) target serotonin to help
restore balance.
○ Norepinephrine: Often associated with alertness and arousal, norepinephrine
also plays a role in mood regulation. Lower levels or dysregulated norepinephrine
 pathways are associated with low energy and attention, which are common in
depression.
○ Dopamine: Known for its role in reward, motivation, and pleasure, dopamine
dysregulation can lead to anhedonia (loss of interest or pleasure in life) and low
motivation. This may be why many people with depression struggle to find joy in
activities they once enjoyed.
● 2. Receptor Sensitivity Changes
○ Over time, neurons may become less sensitive or desensitized to certain
neurotransmitters due to prolonged exposure to high or low levels of these
chemicals. This can happen with serotonin, dopamine, or norepinephrine.
Reduced sensitivity of receptors can contribute to mood regulation problems,
making it difficult for people to experience positive or stable moods.
● 3. HPA (Hypothalamic-Pituitary-Adrenal) Axis Dysfunction
○ Chronic stress and dysregulation of the HPA axis, which controls the body's
stress response, can elevate cortisol levels (the stress hormone). Excessive
cortisol can lead to inflammation and interfere with neurotransmitter function,
particularly serotonin and dopamine, both of which are essential for mood
regulation.
○ Prolonged exposure to high cortisol levels can also reduce neurogenesis (the
formation of new neurons) in the hippocampus, a brain region critical for memory
and emotion processing. This reduction can worsen depression symptoms.
● 4. Inflammation and Immune System Dysregulation
○ Inflammation has been linked to depression, with research showing that some
individuals with depression have higher levels of inflammatory markers. Chronic
inflammation can impact neurotransmitter metabolism and impair brain function.
○ Inflammatory cytokines (small proteins involved in cell signaling) can cross the
blood-brain barrier, affecting brain regions associated with mood and energy.
They can also alter the metabolism of tryptophan, which is necessary for
serotonin production, leading to lower serotonin levels.
● 5. Neuroplasticity and Brain Structure Changes
○ Depression is associated with reduced neuroplasticity (the brain’s ability to adapt
and form new connections). Stress and certain genetic factors can reduce
neurotrophic factors like BDNF (brain-derived neurotrophic factor), which support
neuron health and growth.
○ Low BDNF levels and reduced neurogenesis are thought to contribute to the
atrophy of brain regions like the hippocampus and prefrontal cortex in individuals
with chronic depression, affecting memory, decision-making, and emotional
regulation.
● 6. Genetic and Epigenetic Factors
○ Genetic predisposition can affect how neurotransmitters are processed and how
sensitive individuals are to changes in neurotransmitter levels. Certain gene
variations may affect serotonin transporter function or increase vulnerability to
stress, making some people more prone to depression.
 ○ Epigenetic changes, which are influenced by environment and experience, can
alter gene expression. For example, exposure to chronic stress or trauma can
lead to changes in gene expression that affect neurotransmitter systems and
increase the risk of developing depression.
● 7. Environmental and Psychological Factors
○ Life stressors, trauma, and lack of social support can contribute to prolonged
periods of stress, triggering biological changes. These factors can exacerbate
chemical imbalances or make it harder for the brain to restore balance.
○ Certain cognitive patterns, such as rumination or negative thinking, can also
perpetuate depressive symptoms, as mental states can have biochemical effects,
influencing neurotransmitter levels and stress responses.
● In summary, while imbalances in neurotransmitters like serotonin, norepinephrine, and
dopamine play a role in depression, they are part of a larger web of factors, including
genetics, stress responses, inflammation, and neuroplasticity. This complexity is why
treatments for depression often include a combination of medication, therapy, lifestyle
changes, and, in some cases, other interventions to address multiple aspects of the
disorder.
○ How does the treatment of depression involving Serotonin-reuptake inhibitors
(SSRI) actually help treat it?
Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed for
depression and work by altering serotonin levels in the brain. Here’s a breakdown
of how SSRIs function and how they help alleviate depressive symptoms:
1. Increasing Serotonin Levels in the Synapse
■ SSRIs target a protein called the serotonin transporter, which is
responsible for reabsorbing serotonin from the synaptic cleft (the gap
between neurons) back into the presynaptic neuron (the neuron releasing
serotonin).
■ By blocking this transporter, SSRIs reduce the reuptake of serotonin,
allowing more serotonin to remain in the synaptic cleft and be available to
bind to receptors on the postsynaptic neuron (the neuron receiving the
signal).
■ This increase in available serotonin helps enhance serotonin signaling,
which is believed to improve mood and reduce symptoms of depression.
○ 2. Gradual Adaptation and Receptor Sensitivity
■ Over time, the increased availability of serotonin in the synapse
encourages adaptive changes in serotonin receptors on the
postsynaptic neuron.
■ Receptors on the postsynaptic neuron may become more sensitive or
increase in number in response to the higher serotonin levels, enhancing
the neuron’s response to serotonin.
■ These gradual changes contribute to long-term improvements in mood
and other depressive symptoms, even though SSRIs don’t have an
immediate effect. It typically takes 2 to 6 weeks for patients to notice
significant improvements.
 ○ 3. Modulating Other Neurotransmitter Systems
■ Although SSRIs primarily target serotonin, they also have indirect effects
on other neurotransmitters. For example, increased serotonin levels
can influence dopamine and norepinephrine activity, which can help
improve motivation, energy, and concentration.
■ These broader effects help address the various symptoms of depression,
which often go beyond just low mood to include lack of motivation,
energy, and interest in life.
○ 4. Supporting Neuroplasticity and Brain Health
■ Chronic stress and depression can reduce levels of BDNF (brain-derived
neurotrophic factor), which is important for neuron growth and brain
plasticity. Low BDNF levels are linked to reduced neurogenesis (the
creation of new neurons) and shrinkage of brain regions like the
hippocampus, which is involved in memory and emotional regulation.
■ SSRIs have been shown to increase BDNF production over time,
promoting neurogenesis and improving neuroplasticity. This helps repair
some of the damage caused by chronic stress and depression and may
help restore healthier brain function over time.
○ 5. Reducing the Stress Response
■ Increased serotonin levels from SSRIs can help regulate the
hypothalamic-pituitary-adrenal (HPA) axis, which controls the body’s
stress response.
■ Depression is often linked to excessive cortisol (the stress hormone),
which can exacerbate symptoms. By stabilizing serotonin levels, SSRIs
can help modulate the HPA axis and reduce overactivity of the stress
response, helping people better manage stress and anxiety.
○ 6. Alleviating Physical Symptoms of Depression
■ Depression often involves physical symptoms like fatigue, changes in
sleep, and appetite disturbance, which are also linked to serotonin.
■ By increasing serotonin signaling, SSRIs can help improve sleep
patterns, appetite, and energy levels, contributing to an overall
improvement in mood and well-being.
○ In Summary
SSRIs help treat depression by boosting serotonin availability in the brain
and allowing for stronger serotonin signaling. This doesn’t just improve mood; it
also promotes brain plasticity, reduces stress, and enhances overall mental and
physical resilience. However, the delayed onset of SSRIs’ effects reflects the time
it takes for the brain to adapt and for longer-term changes, such as increased
neuroplasticity, to take place.
● Additional: what is lateral inhibition?
Lateral inhibition is a process in the nervous system where neurons inhibit the activity of
their neighboring neurons. This mechanism enhances contrast and sharpens sensory
 perception by amplifying differences between adjacent signals.
How Lateral Inhibition Works
○ Signal Detection: When a sensory receptor (such as a photoreceptor in the eye
or a touch receptor in the skin) is stimulated by a specific stimulus (like light or
pressure), it sends an excitatory signal to a corresponding neuron.
○ Neighboring Inhibition: At the same time, the stimulated neuron sends
inhibitory signals to neighboring neurons, either directly or through intermediate
neurons called interneurons.
○ Contrast Enhancement: The inhibition of neighboring neurons suppresses
weaker signals in the surrounding area, which enhances the relative strength of
the central (or main) signal. This makes the original signal stand out more clearly
against the background.
● Importance of Lateral Inhibition
○ Enhances Sensory Contrast: By emphasizing the difference between adjacent
signals, lateral inhibition allows the nervous system to detect edges, borders, and
contrasts more clearly. For example, in vision, it helps in detecting edges and
patterns, which is crucial for recognizing objects and shapes.
○ Improves Spatial Resolution: In sensory systems like touch and vision, lateral
inhibition increases spatial resolution, making it easier to distinguish two closely
located stimuli.
○ Sharpens Perception: Lateral inhibition prevents overstimulation by dampening
redundant signals, which can help the brain focus on key information.
● Examples of Lateral Inhibition
○ Vision: In the retina, photoreceptor cells inhibit neighboring cells through a
network of interneurons (horizontal and amacrine cells). This enhances contrast
at the edges of objects, helping us to detect shapes and contours.
○ Touch: In the somatosensory system, when a pressure point on the skin is
stimulated, the receptors inhibit neighboring receptors, making the perception of
that pressure point more defined.
● In summary, lateral inhibition is a neural process that sharpens sensory input by
suppressing surrounding signals, making the main signal more distinct. This is essential
for accurate perception in systems like vision, touch, and hearing.

Physiology of neurons
● Neurons are essential for communication within the nervous system.
● The lecture begins with a discussion about the importance of the lipid bilayer, which acts
as a boundary between the inside and outside of the cell.
● The lecture then delves into the evolution of the lipid bilayer and how it was formed.
● The lecture also mentions the role of biomolecules in the formation of the lipid bilayer,
which were found on meteors.
● Neuron Structure and Function
 ○ The neuron's membrane is composed of lipids and proteins, including ion
channels.
○ Ion channels are crucial for generating the resting and action potentials.
○ The lecture uses the example of Paramecium to illustrate the presence of ion
channels in simple organisms.
○ Paramecium exhibits different behaviors based on the location of ion channels in
its body.
○ The lecture emphasizes that ion channels have been present in cells for a long
time, even before the evolution of neurons.
○ The lecture then discusses the different types of neurons, including multipolar,
bipolar, and unipolar neurons.
○ The lecture provides examples of where these different types of neurons are
found in the human body.
○ The lecture also highlights a recent study that mapped the entire connectome of
the fruit fly brain.
○ The lecture emphasizes that insect brains are structured differently than human
brains.
● Resting Potential
○ The resting potential is the electrical potential difference across the neuron's
membrane when it is not transmitting a signal.
○ The resting potential is primarily determined by the concentration gradient of
potassium ions.
○ The lecture explains that potassium ions flow through open potassium channels,
driven by the concentration gradient.
○ The lecture also mentions the role of the electrical gradient, which pulls
potassium ions back into the cell.
○ The lecture introduces the Nernst equation, which is used to calculate the
equilibrium potential for a single ion.
○ The lecture also mentions the Goldman-Hodgkin-Katz equation, which is used to
calculate the membrane potential when multiple ions are present.
○ The lecture emphasizes the importance of the sodium-potassium pump in
maintaining the resting potential.
○ The lecture also discusses the consequences of disrupting the ion concentration
balance, such as cell swelling or shrinking.
○ The lecture provides practical advice on hydration and avoiding excessive salt
intake.
● Action Potential
○ The action potential is a rapid, short-lasting change in the electrical potential
difference across the neuron's membrane.
○ The lecture explains that the action potential is triggered by a depolarization of
the membrane, which opens voltage-gated sodium channels.
○ The lecture describes the different phases of the action potential, including
depolarization, repolarization, and hyperpolarization.
 ○ The lecture also mentions the refractory period, which is a brief period after an
action potential during which another action potential cannot be generated.
○ The lecture explains that the absolute refractory period is caused by the
inactivation of voltage-gated sodium channels.
○ The lecture introduces the Hodgkin-Huxley cycle, which describes the positive
feedback loop that amplifies the depolarization during the action potential.
○ The lecture explains that voltage-gated potassium channels open with a delay,
contributing to repolarization.
○ The lecture discusses the role of the sodium-potassium pump in restoring the ion
concentration balance after an action potential.
○ The lecture also explores the consequences of altering the kinetics of ion
channels.
● Action Potential Propagation
○ The action potential travels along the axon, transmitting information from one
neuron to another.
○ The lecture explains that in myelinated axons, the action potential jumps from
one node of Ranvier to the next, a process called saltatory conduction.
○ The lecture emphasizes that saltatory conduction is much faster than continuous
conduction.
○ The lecture also mentions that the speed of action potential propagation is
affected by the thickness and myelination of the axon.
○ The lecture contrasts the propagation of action potentials with the propagation of
graded potentials, which are localized and decay over distance.
● Synaptic Transmission
○ The lecture briefly introduces synaptic transmission, which is the process by
which neurons communicate with each other.
○ The lecture mentions that the next part of the course will cover the synapse and
neural transmission in more detail.
● Neurotransmission Overview
○ Key Concepts
■ EPSPs and IPSPs: Excitatory postsynaptic potentials (EPSPs) and
inhibitory postsynaptic potentials (IPSPs) are crucial in determining
whether an action potential will fire. EPSPs are positive changes in
membrane potential, while IPSPs are negative changes .
■ Decremental Signals: The strength of signals decreases with distance.
For instance, an EPSP far from the axon hillock may not trigger an action
potential due to the decremental nature of the signal .
■ Action Potential Initiation: The location of axons and the strength of
incoming signals affect whether an action potential is triggered. Signals
closer to the axon hillock have a greater impact .
○ Neurotransmission Process
■ Synapse Structure: The synapse consists of a presynaptic terminal (axon
terminal) and a postsynaptic terminal (dendrite). Neurotransmitters are
stored in vesicles within the presynaptic terminal .
 ■ Calcium's Role: When an action potential reaches the presynaptic
terminal, voltage-gated calcium channels open, allowing calcium ions to
enter. This influx is crucial for vesicle fusion and neurotransmitter release
.
■ Vesicle Fusion Mechanisms:
■ Kiss-and-Run: Vesicles briefly fuse with the membrane to release
some neurotransmitter and then recycle .
■ Merge and Recycle: Vesicles fully fuse with the membrane,
releasing all neurotransmitter content, followed by endocytosis to
recycle membrane .
○ Neurotransmitter Types
■ Acetylcholine: Involved in muscle control and has two receptor types:
nicotinic (ionotropic) and muscarinic (metabotropic) .
■ Monoamines: Includes serotonin, dopamine, and norepinephrine, which
are small molecules with various functions in the nervous system .
■ Amino Acids: Glutamate is excitatory, while GABA is inhibitory, both
acting quickly and locally .
■ Receptor Types
■ Ionotropic Receptors: These are ligand-gated ion channels that
open upon neurotransmitter binding, leading to rapid changes in
membrane potential .
■ Metabotropic Receptors: These receptors activate G-proteins and
initiate a cascade of intracellular events, leading to slower but
more diverse cellular responses .
○ Drug Interactions
■ Agonists and Antagonists:
■ Agonists mimic neurotransmitters and activate receptors.
■ Antagonists block receptors and prevent neurotransmitter action .
■ Inverse Agonists: These have the opposite effect of agonists, reducing
the baseline activity of receptors .
■ Competitive vs. Non-competitive Antagonists: Competitive antagonists vie
for the same binding site as neurotransmitters, while non-competitive
antagonists bind elsewhere, affecting receptor function regardless of
neurotransmitter presence .
● Neuromodulators: These are neurotransmitters that have more diffuse and longer-lasting
effects on neuronal excitability and synaptic transmission .

Neuroscientific methods in brain studies

● What are the different ways to measure activity in the brain and portray certain brain
structures (brain imaging)? (graph: various dimensions of neuroscience methods on
pebblepad)
There are several techniques for measuring brain activity and visualizing brain
structures. Each method offers unique insights into the brain’s functioning and structure
by targeting different dimensions like spatial and temporal resolution, invasiveness, and
type of data collected. Here's an overview of the main brain imaging techniques and how
they fit into the various dimensions of neuroscience.
Brain Imaging Techniques: Structural vs. Functional
○ Structural Imaging Techniques
■ These methods primarily capture detailed images of brain structures and
are used to assess anatomy, locate lesions, and monitor physical
changes in the brain.
■ Magnetic Resonance Imaging (MRI):
■ What it Measures: High-resolution images of brain anatomy.
■ Spatial Resolution: Excellent (1-2 mm).
■ Temporal Resolution: Not applicable (static images).
■ Invasiveness: Non-invasive.
■ Applications: Used for diagnosing tumors, structural
abnormalities, and brain injury.
■ Computed Tomography (CT):
■ What it Measures: Brain structure through X-ray images.
■ Spatial Resolution: Good (up to 5 mm), but less detailed than
MRI.
■ Temporal Resolution: Not applicable (static images).
■ Invasiveness: Minimally invasive (uses ionizing radiation).
■ Applications: Commonly used in emergency settings to detect
bleeding, fractures, or tumors.
○ Functional Imaging Techniques
■ These methods capture changes in brain activity, typically through
indicators like blood flow, electrical activity, or metabolism, allowing
researchers to observe brain function in real-time.
■ Functional Magnetic Resonance Imaging (fMRI):
■ What it Measures: Changes in blood flow and oxygenation
(BOLD signal)
■ The blood-oxygen-level-dependent (BOLD) signal,
detected in fMRI, reflects changes in deoxyhemoglobin
driven by localized changes in brain blood flow and blood
oxygenation, which are coupled to underlying neuronal
activity by a process termed neurovascular coupling. as
proxies for neural activity.
■ Spatial Resolution: Very good (1-2 mm).
■ Temporal Resolution: Moderate (seconds).
■ Invasiveness: Non-invasive.
■ Applications: Studying brain regions involved in tasks like
memory, emotion, and movement.
■ Positron Emission Tomography (PET):
■ What it Measures: Metabolic activity using radiotracers.
 ■ Spatial Resolution: Good (4-5 mm).
■ Temporal Resolution: Poor (minutes).
■ Invasiveness: Moderately invasive (requires radioactive tracers).
■ Applications: Used in research and clinical diagnostics,
especially for studying brain diseases like Alzheimer's.
■ Electroencephalography (EEG):
■ What it Measures: Electrical activity on the scalp produced by
neuronal activity.
■ Spatial Resolution: Low (cm-level precision).
■ Temporal Resolution: Excellent (milliseconds).
■ Invasiveness: Non-invasive.
■ Applications: Widely used in diagnosing epilepsy, sleep studies,
and cognitive research on attention, perception, and
decision-making.
■ Magnetoencephalography (MEG):
■ What it Measures: Magnetic fields generated by neuronal activity.
■ Spatial Resolution: Moderate (mm-level).
■ Temporal Resolution: Excellent (milliseconds).
■ Invasiveness: Non-invasive.
■ Applications: Used for mapping brain activity, especially in
studying sensory processing, language, and motor control.
■ Near-Infrared Spectroscopy (NIRS):
■ What it Measures: Changes in blood oxygenation, similar to fMRI
but through near-infrared light.
■ Spatial Resolution: Moderate (cm-level).
■ Temporal Resolution: Moderate (seconds).
■ Invasiveness: Non-invasive.
■ Applications: Primarily used in infants or populations where fMRI
isn’t practical, often for language and developmental studies.
○ Invasive Techniques
■ These methods involve direct measurement or stimulation of brain activity
and are used in specific research or clinical contexts.
■ Single-Unit Recording:
■ What it Measures: Electrical activity from individual neurons.
■ Spatial Resolution: Excellent (cellular level).
■ Temporal Resolution: Excellent (milliseconds).
■ Invasiveness: Highly invasive.
■ Applications: Primarily used in animal research or with patients
undergoing brain surgery.
■ Electrocorticography (ECoG):
■ What it Measures: Electrical activity from the cortical surface.
■ Spatial Resolution: High (mm-level).
■ Temporal Resolution: Excellent (milliseconds).
■ Invasiveness: Moderately invasive (requires craniotomy).
 ■ Applications: Used in surgical planning for epilepsy patients and
brain-computer interface research.
○ Visualization: Various Dimensions of Neuroscience Methods (Graph Explanation)
A typical graph for "various dimensions of neuroscience methods" might plot
spatial resolution on the x-axis and temporal resolution on the y-axis. Each
technique would be represented by a point or bubble, indicating where it falls
within these dimensions:
■ High Spatial, High Temporal: Ideal but rare; single-unit recordings are
closest.
■ High Spatial, Low Temporal: Structural MRI and CT fall here, ideal for
detailed anatomy but not for tracking fast changes.
■ Moderate Spatial, High Temporal: EEG and MEG, capturing fast brain
dynamics but with less spatial detail.
■ Moderate Spatial, Moderate Temporal: fMRI, which captures both
structure and function with good spatial resolution but moderate temporal
precision.
○ This kind of graph illustrates how different brain imaging techniques complement
each other by providing insights along various dimensions of brain structure and
function.
○ What are their strengths and weaknesses?
Techniqu Spatial Temporal Invasiveness Cost and
e Resolution Resolution Practicality

MRI Excellent Not applicable Non-invasive Expensive, widely

available

fMRI Good Moderate Non-invasive Expensive, widely

available

PET Moderate Poor Moderately Very expensive,

invasive limited access

EEG Low Excellent Non-invasive Low-cost, portable

MEG Moderate Excellent Non-invasive Very expensive,

limited access

NIRS Moderate Moderate Non-invasive Low to moderate

cost, portable

Single-Unit Excellent Excellent Highly Limited to research

invasive settings

ECoG High Excellent Moderately Used in specific

invasive clinical cases
●
What is MRI and how does it work?
MRI, or Magnetic Resonance Imaging, is a non-invasive medical imaging technique
used to create detailed images of the organs and tissues inside the body. It’s commonly
used to diagnose and monitor various medical conditions, especially those involving the
brain, spinal cord, muscles, joints, and blood vessels.
Here’s a simplified explanation of how MRI works:
○ Magnetic Field: MRI uses a powerful magnetic field to align the hydrogen
protons in the water molecules of your body. Hydrogen atoms are abundant in
the human body, especially in soft tissues, and respond well to magnetic fields.
○ Radio Waves: Once the protons are aligned, a pulse of radio waves is sent
through the body. This pulse disturbs the alignment of the protons.
○ Relaxation: After the radio wave pulse is turned off, the protons slowly return to
their aligned state within the magnetic field. As they do, they emit radio signals.
○ Detection and Image Creation: These emitted signals are detected by the MRI
scanner and are processed by a computer to generate detailed cross-sectional
images of the body. These images can then be assembled into 3D images for a
comprehensive view of the area of interest.
● MRI is highly valued in the medical field because it provides clear images of soft tissues
without using ionizing radiation, as X-rays and CT scans do. This makes it a safer option
for many types of examinations, especially when repeated imaging is necessary.
● What is an EEG (Electroencephalogram) and how does it work?
An EEG, or Electroencephalogram, is a test that measures electrical activity in the brain.
It’s commonly used to diagnose and monitor conditions that affect brain function, such as
epilepsy, sleep disorders, head injuries, and brain tumors.
Here’s how EEG works:
○ Electrode Placement: Small metal discs with thin wires, called electrodes, are
placed on the scalp. These electrodes detect the tiny electrical signals produced
by brain cells (neurons) as they communicate.
○ Signal Detection: Neurons in the brain communicate via electrical impulses, and
these impulses create patterns of brain waves that vary depending on a person’s
level of consciousness, state of relaxation, or response to stimuli. The electrodes
capture these electrical impulses without transmitting any electricity into the
brain.
○ Data Recording: The electrical activity picked up by the electrodes is amplified
and recorded by a computer as wavy lines on a screen or as a printed output.
These waves have different frequencies, and they’re categorized into types, like
alpha, beta, delta, and theta waves, each associated with different brain activities
or states.
○ Analysis: A specialist interprets the patterns in the recorded brain waves to
diagnose or monitor conditions. For instance, unusual patterns or sudden bursts
of electrical activity can indicate epilepsy, while slower waves might suggest brain
injury or inflammation.
● EEG is non-invasive and painless, and it provides real-time data on brain function. It’s
particularly useful for identifying abnormal brain wave patterns and monitoring changes
in brain activity over time.
● How do we measure glucose levels in the brain and what are those measures used for?
Measuring glucose levels in the brain can give valuable insights into brain metabolism
and function, as glucose is the primary energy source for brain cells. Here are some of
the methods used to measure brain glucose levels and their applications:
1. Positron Emission Tomography (PET) Scans
○ How It Works: PET scans measure glucose metabolism in the brain by injecting
a small amount of a radioactive glucose tracer, typically fluorodeoxyglucose
(FDG), into the bloodstream. This tracer behaves like glucose but can be
detected by the PET scanner.
○ Purpose: By tracking where and how much of this tracer accumulates in the
brain, PET scans provide a map of glucose utilization. Areas of higher or lower
glucose uptake indicate areas of more or less brain activity.
○ Applications: PET scans are used in diagnosing and monitoring neurological
conditions like Alzheimer’s disease, epilepsy, and brain tumors, where certain
brain regions may show abnormal glucose metabolism.
● 2. Magnetic Resonance Spectroscopy (MRS)
○ How It Works: MRS, an add-on technique to MRI, can detect specific chemicals
in the brain, including glucose and related metabolites. It does so by analyzing
the magnetic properties of these molecules.
○ Purpose: MRS gives a more localized view of glucose concentrations and can
track changes in real-time without radioactive tracers.
○ Applications: MRS is used to study brain metabolism in conditions like traumatic
brain injury, schizophrenia, and even metabolic disorders that affect the brain.
● 3. Cerebral Microdialysis
○ How It Works: This is an invasive method, typically used in research or intensive
care, where a thin probe is inserted into the brain tissue. The probe samples
extracellular fluid, including glucose, allowing direct measurement of glucose
levels.
○ Purpose: Microdialysis gives a highly localized and real-time view of glucose
levels, which is especially useful for acute brain injuries.
○ Applications: It’s often used in critical care to monitor patients with severe brain
injuries or in research on brain metabolism and neuroprotection.
● Uses of Brain Glucose Measurements
○ Neurological Diagnosis and Monitoring: Helps in detecting and monitoring
conditions like Alzheimer’s, dementia, epilepsy, and brain tumors, where specific
areas may show reduced or increased glucose uptake.
○ Research on Brain Function: Studies how glucose metabolism affects
cognition, memory, mood, and responses to therapies or interventions.
○ Evaluating Brain Injuries: In traumatic brain injuries or stroke, monitoring
glucose can help assess damage and recovery progress.
 ○ Metabolic and Mental Health Studies: Conditions like schizophrenia,
depression, and bipolar disorder often show abnormalities in brain glucose
metabolism. Measurements can help evaluate treatment effectiveness and
understand underlying causes.
● These methods allow for the assessment of brain energy demands and dysfunction,
offering valuable information for both clinical treatment and neurological research.
● What are the methods for modulating brain stimulation (e.g. DBS, TMS, etc.)?
Brain stimulation techniques are used to modulate neural activity for therapeutic,
diagnostic, or research purposes. These methods vary in invasiveness, mechanism, and
applications. Here are some of the most common brain stimulation methods:
1. Deep Brain Stimulation (DBS)
○ How It Works: DBS involves surgically implanting electrodes into specific brain
regions, often connected to a small device (like a pacemaker) under the skin of
the chest. This device sends electrical impulses to modulate brain activity.
○ Applications: DBS is commonly used for treating movement disorders, such as
Parkinson’s disease, essential tremor, and dystonia. It’s also explored for
psychiatric conditions, like obsessive-compulsive disorder (OCD) and
depression.
○ Advantages: DBS allows for targeted, adjustable, and continuous stimulation,
making it effective for chronic conditions.
○ Disadvantages: As an invasive procedure, DBS carries risks like infection,
bleeding, and hardware complications.
● 2. Transcranial Magnetic Stimulation (TMS)
○ How It Works: TMS is non-invasive and uses magnetic fields to generate small
electric currents in targeted brain regions. A magnetic coil is placed against the
scalp, and when activated, it creates magnetic pulses that stimulate the brain.
○ Applications: TMS is widely used to treat major depressive disorder (especially
treatment-resistant depression) and is being researched for other conditions like
anxiety, PTSD, and schizophrenia.
○ Advantages: Non-invasive, well-tolerated, and does not require anesthesia or
surgery. TMS can be adjusted for intensity and frequency to stimulate or inhibit
brain activity.
○ Disadvantages: Limited to surface or near-surface brain regions and may
require multiple sessions for effect. Side effects include mild headaches and
discomfort at the stimulation site.
● 3. Transcranial Direct Current Stimulation (tDCS)
○ How It Works: tDCS is a non-invasive technique where a small, constant
electrical current is applied via electrodes placed on the scalp. This current
modulates the excitability of neurons, making them more or less likely to fire.
○ Applications: tDCS is used experimentally to improve cognitive functions, motor
skills, and memory. It’s also being explored for depression, chronic pain, and
stroke rehabilitation.
○ Advantages: Non-invasive, portable, relatively inexpensive, and easy to
administer.
 ○ Disadvantages: The effects are often subtle and vary significantly among
individuals. It requires precise placement and dose management for optimal
results.
● 4. Transcranial Alternating Current Stimulation (tACS)
○ How It Works: Similar to tDCS, tACS applies electrical stimulation to the scalp
but with alternating rather than direct current. This alternating current can
synchronize with specific brain wave frequencies, potentially influencing brain
rhythms.
○ Applications: tACS is primarily used in research to explore its effects on brain
oscillations and cognitive processes, such as memory, attention, and perception.
○ Advantages: Non-invasive and has the potential to target specific brain wave
frequencies, which may help in studying or modulating brain activity related to
different mental states.
○ Disadvantages: Experimental and not yet widely used clinically; effects can be
inconsistent and are still being researched for safety and efficacy.
● 5. Electroconvulsive Therapy (ECT)
○ How It Works: ECT involves passing a controlled electrical current through the
brain to induce a brief seizure. This is done under anesthesia to minimize
discomfort.
○ Applications: ECT is primarily used to treat severe and treatment-resistant
depression, bipolar disorder, and some types of schizophrenia.
○ Advantages: ECT can be highly effective for individuals who don’t respond to
other treatments, and its benefits often appear faster than medication alone.
○ Disadvantages: ECT can cause temporary memory loss, confusion, and other
cognitive side effects. It requires anesthesia and is generally used as a last-resort
option.
● 6. Responsive Neurostimulation (RNS)
○ How It Works: RNS is an implantable device similar to DBS but has a unique
feature: it continuously monitors brain activity and delivers targeted electrical
pulses only when abnormal activity (like a seizure) is detected.
○ Applications: RNS is used for epilepsy management, particularly for individuals
with drug-resistant epilepsy.
○ Advantages: It’s responsive, so it only delivers stimulation when needed,
potentially reducing side effects and preserving normal brain activity.
○ Disadvantages: Invasive, with surgical risks. It requires precise programming
and monitoring.
● 7. Vagus Nerve Stimulation (VNS)
○ How It Works: VNS involves implanting a device under the skin that sends
electrical pulses to the vagus nerve, which then transmits these signals to the
brain.
○ Applications: Originally developed for epilepsy, VNS is also used to treat
depression, particularly when other treatments haven’t worked.
 ○ Advantages: It provides continuous, indirect brain stimulation without directly
interacting with brain structures.
○ Disadvantages: It’s an invasive procedure with potential side effects like voice
changes, shortness of breath, or throat discomfort.
● Summary of Brain Stimulation Applications:
○ Neurological Disorders: DBS, RNS, and VNS are commonly used to treat
epilepsy, movement disorders, and in some cases, chronic pain.
○ Psychiatric Disorders: TMS, tDCS, ECT, and DBS are applied to treat
treatment-resistant depression, OCD, anxiety, and other psychiatric conditions.
○ Cognitive and Motor Enhancement: tDCS, tACS, and TMS are used
experimentally to enhance cognitive and motor functions in healthy individuals
and in rehabilitation settings.
● Each technique offers unique benefits and challenges, and the choice of method
depends on the condition, treatment goals, and patient profile. These methods are
continuously evolving, with ongoing research aimed at improving their safety, efficacy,
and specificity.
● What was the human circulation balance and how is it related to modern neuro-imaging
techniques (explain the figure on pebblepad)?
The "human circulation balance" refers to an early approach in neuroscience that
measured blood flow to understand brain function. This technique, developed by Angelo
Mosso in the late 19th century, aimed to connect mental activity with changes in blood
circulation in the brain. Mosso's device was a seesaw-like balance that held a person in
a horizontal position. When the subject engaged in mental tasks, such as reading or
performing calculations, the balance would tip due to increased blood flow to the head,
suggesting more blood was moving to active brain areas.
Connection to Modern Neuroimaging Techniques
Mosso’s human circulation balance was a precursor to modern neuroimaging methods
that measure brain activity based on blood flow. Today’s techniques, like Functional
Magnetic Resonance Imaging (fMRI) and Positron Emission Tomography (PET), build on
the principle that regions of the brain that are more active require more oxygen and
energy, which is supplied by increased blood flow. Here’s how they connect:
○ fMRI: Measures brain activity by detecting changes in blood oxygenation. When
a brain region is active, it consumes more oxygen, and the blood flow to that area
increases—a concept first hinted at by Mosso’s observations.
○ PET: Often uses a radioactive tracer that binds to glucose, which is actively
consumed by functioning neurons, allowing researchers to observe which brain
areas are active.
● Explanation of the Figure on PebblePad
In your PebblePad figure, there may be an illustration of Mosso’s balance setup or a
visual comparison between Mosso’s method and modern imaging. Typically, such figures
show the person lying on the balance and emphasize how an increase in brain activity
(and therefore blood flow to the brain) causes a physical shift, demonstrating Mosso’s
findings.
The figure likely demonstrates the historical evolution of neuroimaging: from Mosso’s
 balance detecting shifts in blood distribution to advanced techniques that precisely map
blood flow and brain activity non-invasively. This connection highlights the progression
from foundational ideas to sophisticated, high-resolution imaging methods used in
neuroscience today.

Cognitive Neuroscience Overview

Introduction to Cognitive Neuroscience

● Cognitive neuroscience is a subfield of psychology focused on understanding human

behavior through the lens of brain function. It emerged from the intersection of
psychology and advancements in medical science regarding the nervous system and the
brain .

Importance of the Brain in Psychology

● Understanding human behavior, cognition, and emotions requires knowledge of how the
brain operates, as all psychological processes are rooted in brain activity .

Methods in Cognitive Neuroscience

● The field relies on various methods to study the brain's role in behavior. This includes
both traditional psychological assessments and advanced neuroimaging techniques .

Neuroimaging Techniques

● Functional Magnetic Resonance Imaging (fMRI): A key tool that allows visualization of
brain activity by measuring changes in blood flow related to neural activity. It provides
high spatial resolution and helps identify active brain areas during tasks .
● Electroencephalography (EEG): Offers excellent temporal resolution, capturing rapid
changes in brain activity, although it has lower spatial resolution compared to fMRI .

Limitations of Neuroimaging

● While neuroimaging techniques provide valuable data, they primarily reveal correlations
between brain activity and behavior, not causation. This limitation necessitates careful
interpretation of results .

Causality in Cognitive Neuroscience

● To establish causal relationships, researchers often rely on lesion studies, where brain
damage is correlated with changes in behavior. However, these studies also face
challenges in establishing definitive causality .

Transcranial Magnetic Stimulation (TMS)

 ● TMS is a non-invasive brain stimulation technique that allows researchers to manipulate
brain activity and observe the effects on behavior. It can either enhance or inhibit brain
function, providing insights into causal relationships .

Neuroplasticity

● The brain's ability to adapt and reorganize itself, known as neuroplasticity, is crucial for
learning and recovery from injuries. TMS and other stimulation techniques can harness
this plasticity to facilitate cognitive improvements .

Experimental Design in Cognitive Neuroscience

● Effective experimental design is essential for drawing valid conclusions about

brain-behavior relationships. Researchers must manipulate independent variables (e.g.,
task conditions) while measuring dependent variables (e.g., brain activity) to establish
causal links .

Case Studies and Applications

● Historical case studies, such as Broca's area, illustrate the relationship between specific
brain regions and functions. Modern techniques allow for more precise identification and
manipulation of these areas .

Conclusion

● Cognitive neuroscience combines psychological theory with neurobiological methods to

deepen our understanding of human behavior. The integration of advanced imaging and
stimulation techniques continues to enhance the field's capacity to explore the
complexities of the brain and its influence on cognition and emotion .

Key Concepts in Cognitive Neuroscience and Brain Stimulation

TMS and Visual Processing

● Transcranial Magnetic Stimulation (TMS): A method with high temporal resolution that
can interfere with brain activity at precise moments. This allows researchers to study the
timing of brain area relevance during tasks .
● Visual Area Five: Interfering with this area during motion detection tasks significantly
reduces accuracy, indicating its critical role in processing visual motion .

Mental Imagery Studies

● Mental Clock Task: Participants imagine two clock times and determine which has a
larger angle between the hands. This task reveals the cognitive processes involved in
mental imagery .
 ● Neural Activation: fMRI studies show bilateral parietal activation during the task,
suggesting both hemispheres contribute to mental image generation and spatial
comparison .

Functional Relevance of Brain Areas

● Division of Labor: The left hemisphere is hypothesized to handle image generation,

while the right hemisphere manages spatial comparisons. However, inhibiting the left
hemisphere surprisingly does not affect task performance, suggesting compensatory
mechanisms .
● Compensation Mechanism: When the left hemisphere is lesioned, the right hemisphere
can take over image generation tasks, indicating the brain's adaptability .

Clinical Applications of TMS

● Depression Treatment: TMS is being explored as a treatment for treatment-resistant

depression (TRD). A specific protocol targets the dorsal lateral prefrontal cortex to
modulate activity in the anterior cingulate cortex, which is often hypoactive in depressed
patients .
● Patient Case Study: A patient named Hanneke experienced significant improvement in
her chronic depression after undergoing TMS therapy, highlighting the potential of TMS
in clinical settings .

Attention Control and Brain Stimulation

● Attention Mechanisms: Research indicates that attention can be controlled in space,

with specific brain rhythms (alpha rhythms) linked to attention shifts. TMS can enhance
these rhythms, potentially improving cognitive abilities .
● Stroke Rehabilitation: TMS has shown promise in improving attention in stroke patients
with left neglect, suggesting its utility in rehabilitation settings .

Conclusion

● The integration of various neuroscience methods, including TMS and fMRI, provides
insights into cognitive processes and offers potential therapeutic avenues for
neurological and psychological disorders. The adaptability of the brain and the
effectiveness of TMS in clinical applications underscore the importance of continued
research in cognitive neuroscience.

Attention
● What is attention? -> more detailed definition
Attention is a cognitive process that allows individuals to selectively focus on specific
information or stimuli while ignoring other distractions. It involves the brain's ability to
 allocate resources to perceive, process, and respond to relevant information in the
environment. This process is fundamental to how we interact with the world, enabling us
to prioritize tasks, filter out irrelevant details, and achieve goals effectively.
Key Aspects of Attention:
○ Selective Attention: Focusing on a specific stimulus while excluding others. For
example, listening to one conversation in a noisy room.
○ Sustained Attention: The ability to maintain focus over time on a single task or
stimulus, such as reading a book for an extended period.
○ Divided Attention: Distributing focus across multiple tasks simultaneously, often
referred to as multitasking.
○ Shifting Attention: The capacity to switch focus from one task or stimulus to
another, adapting to changing priorities or demands.
○ Involuntary Attention: Automatic attention drawn to stimuli due to their intensity
or relevance, such as a loud noise or a bright light.
○ Voluntary Attention: Conscious and deliberate focus on a task or object, guided
by personal goals or interests.
● Neural Mechanisms:
Attention is regulated by networks in the brain, primarily involving:
○ The prefrontal cortex, which is responsible for planning and decision-making.
○ The parietal cortex, which processes sensory information and spatial
awareness.
○ The thalamus, which acts as a relay station for sensory signals.
○ The reticular activating system (RAS), which modulates alertness and arousal.
● Importance of Attention:
○ Facilitates learning and memory by ensuring that relevant information is
processed and encoded.
○ Enhances productivity and efficiency by helping focus on critical tasks.
○ Enables safety and survival by allowing quick responses to significant
environmental changes.
● Attention can vary in intensity and duration, influenced by factors such as fatigue,
interest, health, and external stimuli. Disorders like ADHD (Attention Deficit Hyperactivity
Disorder) illustrate how challenges with attention can impact daily functioning.
● What different types of attention exist?
1. Selective Attention
○ Definition: Focusing on one specific stimulus while ignoring others.
○ Example: Listening to one conversation in a noisy room (known as the "cocktail
party effect").
○ Purpose: Helps filter out irrelevant information to concentrate on what is
important.
●
2. Sustained Attention (Vigilance)
○ Definition: Maintaining focus on a task or stimulus over an extended period.
○ Example: Watching a long movie or monitoring a radar screen for hours.
 ○ Purpose: Essential for tasks requiring prolonged concentration.
●
3. Divided Attention (Multitasking)
○ Definition: Splitting focus across multiple tasks or stimuli simultaneously.
○ Example: Driving while talking on the phone (though this can reduce
performance).
○ Purpose: Allows for managing multiple tasks, but may decrease the efficiency of
each.
●
4. Alternating Attention (Task-Switching)
○ Definition: The ability to shift focus between two or more tasks or stimuli.
○ Example: Cooking while periodically checking your phone for messages.
○ Purpose: Enables flexibility in adapting to changing priorities or demands.
●
5. Focused Attention
○ Definition: A brief, intense concentration on a single stimulus or task.
○ Example: Responding to a sudden loud noise or an unexpected question.
○ Purpose: Quickly identifies and reacts to significant stimuli.
●
6. Executive Attention
○ Definition: Managing attention resources in tasks involving planning,
decision-making, or problem-solving.
○ Example: Creating a detailed project plan while prioritizing tasks and avoiding
distractions.
○ Purpose: Governs goal-directed behavior and complex mental tasks.
●
7. Perceptual Attention
○ Definition: Focusing on specific sensory input, such as sights or sounds.
○ Example: Watching for a specific color or listening for a particular word in a
conversation.
○ Purpose: Filters sensory information relevant to the situation.
●
8. Involuntary (Bottom-Up) Attention
○ Definition: Automatically drawn to a stimulus without conscious effort.
○ Example: Turning to look at a flashing light or loud noise.
○ Purpose: Ensures quick reactions to potentially important or threatening stimuli.
●
9. Voluntary (Top-Down) Attention
○ Definition: Intentionally directing focus based on goals or interests.
○ Example: Concentrating on studying for an exam despite background noise.
○ Purpose: Allows for purposeful and goal-driven focus.
●
10. Spatial Attention
 ○ Definition: Focusing on a specific location or region in the environment.
○ Example: Watching a soccer player in a match to predict their next move.
○ Purpose: Enhances the ability to track movement and anticipate changes in the
environment.
●
11. Temporal Attention
○ Definition: Focusing attention on specific moments in time.
○ Example: Timing your reaction to a green light while driving.
○ Purpose: Helps process and respond to stimuli occurring in predictable or critical
time frames.
●
Disorders Related to Attention:
○ ADHD (Attention Deficit Hyperactivity Disorder): Impaired ability to sustain
attention or control impulses.
○ Neglect Syndrome: Difficulty attending to one side of space, often due to brain
damage.
○ Dyslexia: Challenges with selective attention to written text.
● How does the spatial cueing task work? -> expected outcomes
The spatial cueing task, often associated with Michael Posner's cueing paradigm, is a
psychological experiment designed to study spatial attention. It reveals how attention is
directed to specific locations in space and how this affects reaction times and accuracy
in detecting or identifying stimuli.

How the Spatial Cueing Task Works

○ Setup:
■ Participants view a screen with a central fixation point.
■ Potential target locations are usually to the left or right of the fixation
point.
○ Procedure:
■ Cue Phase: A cue (e.g., an arrow, a highlight, or a flash) is presented,
indicating where a target might appear.
■ Valid Cue: Correctly predicts the target's location.
■ Invalid Cue: Directs attention to the wrong location.
■ Neutral Cue: Provides no information about the target's location.
■ Target Phase: After a brief delay (stimulus onset asynchrony, SOA), a
target (e.g., a symbol or shape) appears in one of the possible locations.
■ Response Phase: Participants respond as quickly as possible by
pressing a button or identifying the target.
○ Manipulations:
■ Cue validity (valid, invalid, neutral).
■ Cue-target onset timing (short or long delays).
■ Target location (left, right, or central).
●
Expected Outcomes
○ Reaction Time (RT) and Accuracy:
■ Valid Cues: Faster reaction times and higher accuracy because the cue
directs attention to the correct location.
■ Invalid Cues: Slower reaction times and lower accuracy due to the need
to reorient attention to the target's actual location.
■ Neutral Cues: Intermediate reaction times and accuracy, as no guidance
is provided.
○ Attention Effects:
■ Demonstrates the benefits of directing attention to relevant locations
(valid cues).
■ Highlights the costs of misdirected attention (invalid cues).
○ Cueing Benefits and Costs:
■ Benefit: The performance boost observed for valid cues compared to
neutral cues.
■ Cost: The performance drop for invalid cues compared to neutral cues.
○ Temporal Dynamics:
■ Short SOAs (e.g., <200ms): Attention is still captured by the cue, and
valid cues show strong benefits.
■ Long SOAs (e.g., >300ms): Effects may diminish or reverse due to
phenomena like inhibition of return (IOR), where attention avoids
revisiting previously cued locations.
○ Peripheral vs. Central Cues:
■ Peripheral cues (e.g., flashes) tend to attract attention reflexively
(bottom-up).
■ Central cues (e.g., arrows) rely on voluntary attention shifts (top-down).
●
Implications and Insights
○ Attention Allocation: Confirms that attention can be directed to specific spatial
locations, even without moving the eyes.
○ Top-Down vs. Bottom-Up Processes: Differentiates between voluntary and
automatic attention shifts.
○ Applications:
■ Understanding attentional deficits (e.g., in ADHD or neglect syndrome).
■ Designing interfaces or alerts that effectively capture attention.
■ Investigating neural mechanisms of attention.
● In summary, the spatial cueing task is a foundational tool in cognitive psychology and
neuroscience, showing how spatial attention influences the speed and accuracy of
responses to visual stimuli.
● What structures/parts of the brain are involved in attention?
Key Brain Structures Involved in Attention
1. Prefrontal Cortex (PFC)
 ○ Role: Central in executive attention, decision-making, and goal-oriented focus.
○ Specific Functions:
■ Directs attention based on goals or intentions.
■ Helps switch attention between tasks (alternating attention).
○ Example: Planning a project and ignoring distractions.
●
2. Parietal Cortex
○ Role: Critical for spatial attention and sensory integration.
○ Specific Functions:
■ Processes where objects are located in space.
■ Directs focus to important sensory inputs.
○ Example: Tracking a moving object like a ball during a game.
●
3. Anterior Cingulate Cortex (ACC)
○ Role: Involved in conflict monitoring and error detection.
○ Specific Functions:
■ Resolves competition between stimuli.
■ Regulates shifts in attention.
○ Example: Resolving distraction when trying to concentrate in a noisy
environment.
●
4. Thalamus
○ Role: Acts as a sensory relay station, directing sensory information to relevant
brain areas.
○ Specific Functions:
■ Filters and prioritizes sensory inputs for attention.
■ Aids in sustained attention by amplifying important signals.
○ Example: Noticing a specific voice in a crowded room.
●
5. Reticular Activating System (RAS)
○ Role: Regulates arousal and alertness, ensuring readiness to pay attention.
○ Specific Functions:
■ Maintains wakefulness and overall alertness.
■ Filters incoming sensory information to highlight what requires focus.
○ Example: Alerting you to a sudden noise while you’re drowsy.
●
6. Basal Ganglia
○ Role: Involved in filtering out irrelevant distractions and supporting
task-switching.
○ Specific Functions:
■ Helps focus on tasks by reducing interference from unnecessary stimuli.
○ Example: Ignoring background chatter while working on an assignment.
●
7. Superior Colliculus (in the Midbrain)
○ Role: Directs attention to visual stimuli.
○ Specific Functions:
■ Coordinates rapid eye movements (saccades) to focus on new objects.
■ Aids in shifting visual attention.
○ Example: Quickly looking at a moving car in your peripheral vision.
●
8. Insular Cortex
○ Role: Integrates external sensory input with internal states (e.g., emotions).
○ Specific Functions:
■ Facilitates awareness of changes in the environment.
■ Supports selective attention to emotionally relevant stimuli.
○ Example: Paying more attention to a friend’s voice when they sound distressed.
●
9. Hippocampus
○ Role: Contributes indirectly by linking attention with memory.
○ Specific Functions:
■ Helps recall relevant information for focused tasks.
■ Supports sustained attention by associating tasks with past experiences.
○ Example: Staying focused on a familiar route based on memory cues.
●
Brain Networks Supporting Attention
○ Dorsal Attention Network (DAN)
■ Includes the parietal and frontal areas.
■ Controls goal-directed (top-down) attention.
■ Example: Searching for a friend in a crowd.
○ Ventral Attention Network (VAN)
■ Involves the temporal-parietal junction and insula.
■ Governs stimulus-driven (bottom-up) attention.
■ Example: Reacting to a sudden loud sound.
○ Default Mode Network (DMN)
■ Associated with mind-wandering and introspection.
■ Shifts activity when transitioning from internal to external focus.
○ Salience Network
■ Includes the anterior cingulate and insula.
■ Detects important stimuli and shifts attention accordingly.
●
Attention is supported by a network of brain regions, each contributing to different types
of attention, such as focusing on a task, shifting between stimuli, or responding to
sudden changes. The prefrontal cortex, parietal cortex, thalamus, and reticular activating
system are among the most crucial players. Together, these structures form a dynamic
system that adapts to various attentional demands.
● How is eye movement related to attention? Why do a lot of studies focus on central
fixation when studying attention?
Eye movement and attention are deeply interconnected because where we look often
reflects where we direct our cognitive resources. This relationship provides valuable
insights into how attention is allocated and processed. Here’s a breakdown of the
connection and why central fixation is a common focus in attention studies:

Relationship Between Eye Movement and Attention

○ Overt Attention:
■ Definition: Directing attention by physically moving the eyes to focus on a
specific object or location.
■ Example: Looking directly at a traffic light to determine its color.
■ Mechanism: Eye movements (saccades, fixations) align the retina with
areas of interest, allowing detailed visual processing.
○ Covert Attention:
■ Definition: Shifting attention without moving the eyes; focusing mentally
on a peripheral stimulus.
■ Example: Monitoring movement in your peripheral vision while
maintaining eye contact with someone.
■ Mechanism: Neural networks shift attention without altering gaze
direction.
○ Saccades and Fixations:
■ Saccades: Rapid eye movements that shift focus from one point to
another.
■ Fixations: Periods when the eyes remain still, allowing detailed
processing of the visual field.
■ These movements reflect the brain's selection of areas to prioritize based
on attention.
○ Attention Precedes Eye Movement:
■ Studies show that shifts in attention often occur before the eyes move,
suggesting that attention guides eye movements.
■ Example: Deciding to look at a bird in the sky before your eyes physically
move toward it.
●
Why Central Fixation is Used in Attention Studies
○ Control Over Visual Input:
■ Central fixation ensures participants are looking at the same area,
standardizing the visual information they receive.
■ This minimizes variability in stimuli processing due to differences in gaze
position.
○ Decoupling Eye Movements and Attention:
■ By keeping gaze fixed, researchers can isolate covert attention (mental
shifts of focus) from overt attention (eye movements).
 ■ Example: Tracking how participants notice changes in peripheral stimuli
without moving their eyes.
○ Precise Measurement:
■ Eye-tracking devices can more accurately detect subtle shifts in gaze and
attention when the starting point (central fixation) is consistent.
■ Reduces noise in data caused by uncontrolled eye movements.
○ Natural Starting Point:
■ Humans naturally fixate centrally to gather visual information efficiently, as
the center of the retina (fovea) provides the sharpest detail.
■ Starting studies with central fixation reflects this natural behavior.
○ Experimental Paradigms:
■ Many classic attention paradigms (e.g., Posner's cueing task) rely on
central fixation to present peripheral cues or targets.
■ This design enables controlled manipulation of attention shifts while
keeping initial conditions constant.
●
Practical Applications
○ Eye movements and attention studies help in fields like neuroscience,
psychology, marketing, and user-interface design.
○ Central fixation studies are foundational for understanding:
■ How we prioritize visual stimuli.
■ The neural mechanisms of attention.
■ Disorders like ADHD or neglect syndrome.
●
In summary, eye movement provides a window into attentional processes because it
reflects both overt and covert shifts of focus. Central fixation is widely used in studies to
ensure consistency, control, and precision in examining how attention is allocated across
the visual field.
● The effects of attention on brain regions involved in sensory perception.
Attention significantly influences the activity of brain regions involved in sensory
perception, enhancing the processing of relevant stimuli while suppressing irrelevant
information. This modulation occurs across various sensory modalities (e.g., visual,
auditory, tactile) and involves dynamic changes in neural activity, connectivity, and
processing efficiency in sensory and higher-order brain regions.

Key Brain Regions and Their Modulation by Attention

1. Primary Sensory Cortices
○ Visual Cortex (V1):
■ Attention amplifies neural responses to stimuli in the attended region of
the visual field.
■ Example: Increased activity in V1 when focusing on a specific color or
motion.
○ Auditory Cortex (A1):
 ■ Enhanced processing of attended sounds (e.g., a specific voice in a noisy
room).
■ Attention filters out background noise by reducing irrelevant neural
responses.
○ Somatosensory Cortex (S1):
■ Heightened sensitivity to attended tactile stimuli (e.g., focusing on a
vibration on the fingertip).
■ Reduced activity for unattended tactile inputs.
●
2. Higher-Order Sensory Areas
○ Extrastriate Visual Areas (e.g., V4, MT):
■ V4: Enhanced response to features like color and shape when attention is
directed.
■ MT: Increased sensitivity to motion when focusing on moving objects.
○ Auditory Association Areas:
■ Superior temporal gyrus and belt areas show greater activation for
attended complex sounds (e.g., speech or music).
○ Parietal Cortex:
■ Enhances integration of sensory information from multiple modalities.
■ Critical for spatial attention and locating stimuli in the environment.
●
3. Thalamus
○ Acts as a "gatekeeper" for sensory information:
■ Role in Attention:
■ Amplifies signals from attended stimuli.
■ Suppresses irrelevant sensory input before it reaches the cortex.
■ Example: The pulvinar nucleus of the thalamus is heavily involved in
visual attention.
●
4. Prefrontal Cortex
○ Regulates sensory processing by controlling attention allocation:
■ Directs sensory regions to prioritize task-relevant stimuli.
■ Mediates top-down attention, aligning sensory input with goals and
expectations.
●
5. Parietal Cortex
○ Key region in the dorsal attention network:
■ Enhances sensory processing in spatial and feature-based attention.
■ Example: The intraparietal sulcus (IPS) modulates activity in sensory
regions to prioritize stimuli in attended locations.
●
Effects of Attention on Sensory Processing
○ Enhanced Neural Responses:
 ■ Attention increases the amplitude of neural activity in sensory regions,
improving detection and discrimination of stimuli.
■ Example: Greater firing rates in V1 neurons when focusing on a specific
part of the visual field.
○ Improved Signal-to-Noise Ratio:
■ Attention boosts the representation of relevant stimuli while suppressing
irrelevant background noise in sensory cortices.
■ Example: Enhanced clarity of a spoken word in a noisy environment.
○ Feature-Specific Modulation:
■ Attention can selectively enhance processing of specific features (e.g.,
motion, color, pitch).
■ Example: Focusing on red objects increases activity in color-sensitive
areas like V4.
○ Increased Cortical Connectivity:
■ Attention strengthens functional connectivity between sensory areas and
higher-order regions (e.g., prefrontal and parietal cortices).
■ This enables more efficient coordination of sensory processing with
cognitive goals.
○ Temporal Dynamics:
■ Attention accelerates the timing of neural responses in sensory regions,
allowing faster processing of attended stimuli.
■ Example: Shortened response latencies in visual or auditory cortices for
attended stimuli.
○ Suppressive Effects:
■ Attention not only enhances relevant stimuli but actively suppresses
irrelevant or distracting inputs.
■ Example: Reduced activity in auditory cortex for unattended background
noise.
●
Clinical and Practical Implications
○ Clinical Conditions:
■ ADHD: Impaired top-down attention leads to reduced modulation of
sensory regions.
■ Neglect Syndrome: Damage to the parietal cortex disrupts attentional
enhancement of sensory input on one side of space.
■ Autism Spectrum Disorder (ASD): Altered sensory attention processing
may contribute to hypersensitivity or focus issues.
○ Applications:
■ Neurorehabilitation: Enhancing sensory attention to improve perception
in stroke or injury patients.
■ Education: Designing learning environments to minimize distractions and
focus attention.
■ User Experience Design: Leveraging sensory attention in product and
interface design (e.g., using bright colors or sounds to direct focus).
 ●
Conclusion
Attention profoundly shapes sensory perception by modulating neural activity in sensory
and higher-order brain regions. It enhances the processing of relevant stimuli while
suppressing distractions, improving efficiency and accuracy in perception. These effects
are crucial for interacting with the environment and achieving behavioral goals.

Memory
Key Concepts in Memory Formation

● Working Memory: A short-lasting system where information is actively retained for a

limited amount of time, typically a few seconds to half a minute. It requires cognitive
effort to maintain information and is limited to about four to seven items at a time , .
● Long-Term Memory: Information from working memory can transition into long-term
memory, which is a more durable and expansive storage system .
● Hippocampus: A critical region in the brain for long-term memory formation. It is involved
in the transition of information from working memory to long-term memory , .
● Engram: A term coined by Richard Semmon to describe the enduring change in the
neural substrate, resulting from a stimulus, that represents a memory , .
● Long-Term Potentiation (LTP): A process where repeated stimulation of a neuron leads
to an increased response from the postsynaptic neuron. This is thought to be a cellular
mechanism for learning and memory , .

Examples and Walkthroughs

● Memory Retrieval: The act of recalling a memory serves as evidence that something was
stored. For instance, being able to remember the name of an actor from a favorite movie
indicates that the memory was stored and can be retrieved , .
● Memory Localization: Early studies attempted to find a specific location for memory in
the brain, leading to the discovery of the hippocampus's role in memory formation , .
● Patient H.M.: A case study that significantly contributed to the understanding of the
hippocampus's role in memory. After surgical removal of the hippocampus to treat
epilepsy, H.M. developed amnesia, indicating the hippocampus's importance in forming
new memories , .
● Neural Connectivity: Memory is thought to be stored through changes in the connectivity
between neurons. When neurons are co-activated, they form stronger connections,
which can later be reactivated to retrieve a memory , .
● Memory and Neural Activity: The transition from working memory to long-term memory
involves a shift from active neural representation to changes in connectivity, which is
more efficient and durable , .
General Comments

● Memory's Role in Shaping the Brain: The act of memory formation and retrieval plays a
fundamental role in shaping our brain's structure and function .
● External Memory Aids: The use of external devices for memory storage may impact our
brain's natural ability to organize memory internally .
● Memory in Devices vs. Brain: Unlike electronic devices where memory components can
be pinpointed, the brain's memory storage is more complex and distributed .

Neuroplasticity and Long-Term Potentiation (LTP)

● Short-term Neuroplasticity: A strong presynaptic stimulation leads to a post-synaptic

change that lasts for minutes to a few hours, known as short-term neuroplasticity .
● Molecular Pathways: To understand changes in cell metabolism and biology that allow
neuroplasticity, we consider molecular pathways and neurotransmitter release .
● Synaptic Gap and Neurotransmitters: Neurons are separated by a synaptic gap, with
neurotransmitters bridging the gap to allow for neuroplasticity .
● Receptors and Channels: Neurotransmitters bind to post-synaptic receptors, opening
channels for ions like sodium, potassium, and calcium to flow in .
● AMPA and NMDA Receptors: AMPA receptors allow sodium influx upon glutamate
binding, while NMDA receptors require both glutamate binding and depolarization to
allow ion influx .
● Calcium's Role in LTP: Calcium influx through NMDA receptors activates processes
leading to the mobilization of dormant AMPA receptors to the post-synaptic membrane .
● Long-term Potentiation (LTP): LTP is the increased responsiveness of the post-synaptic
cell to presynaptic input, lasting beyond the initial stimulus for hours .
● Late Phase LTP: Repeated stimulation leads to gene expression and structural changes
in neurons, resulting in long-lasting memory formation .
● Memory Formation: LTP is crucial for memory formation, with sleep playing a key role in
the consolidation of memories .
● Brain Reshaping: Memory formation and learning experiences reshape the brain, with
structural changes occurring in response to new challenges .
● Alzheimer's Disease: Alzheimer's is characterized by toxic neural plaques that destroy
connections and lead to memory loss, with early life stimulation acting as a buffer
against symptoms .
● Active Lifestyle: An active mental and physical life can create a buffer against
neurodegenerative symptoms, even in the presence of Alzheimer's pathology .

Memory (STM)
● What is memory (STM)
Memory refers to the brain's ability to encode, store, and retrieve information. It is
essential for learning, reasoning, and decision-making. Short-term memory (STM) is a
temporary storage system that holds a small amount of information for a brief period,
typically 15-30 seconds. It allows you to keep information in mind while actively using or
manipulating it (e.g., remembering a phone number long enough to dial it).
Key characteristics of STM:
○ Capacity: Limited to 5–9 items (as proposed by George Miller's "magic number 7
± 2").
○ Duration: Short-lived unless actively rehearsed.
○ Function: Essential for tasks like problem-solving, reasoning, and language
comprehension.
○ What are the different types of memory?
■ Sensory Memory:
■ Briefly stores sensory information from the environment.
■ Subtypes:
■ Iconic Memory: Visual information (~0.5 seconds).
■ Echoic Memory: Auditory information (up to 3-4 seconds).
■ Short-Term Memory (STM):
■ Temporary storage for immediate use.
■ If rehearsed, STM may transition into long-term memory.
■ Long-Term Memory (LTM):
■ Durable storage of information.
■ Subtypes:
■ Explicit (Declarative) Memory: Conscious recall
of facts/events.
■ Episodic Memory: Personal experiences.
■ Semantic Memory: General knowledge.
■ Implicit (Non-declarative) Memory: Unconscious
skills and behaviors.
■ Procedural Memory: Skills like riding a
bike.
■ Emotional Conditioning: Learned
emotional responses.
■ Working Memory:
■ An extension of STM, involving active manipulation of information.
■ Includes components like the phonological loop (verbal
information), visuospatial sketchpad (visual/spatial data), and
central executive (coordination).
○ What are the different models/mechanisms of memory?
■ Atkinson-Shiffrin Model (Multi-Store Model):
■ Proposes three distinct stages of memory:
■ Sensory Register: Briefly holds sensory input.
 ■ Short-Term Memory (STM): Temporary
processing/storage.
■ Long-Term Memory (LTM): Permanent storage.
■ Working Memory Model (Baddeley and Hitch):
■ Expands on STM by emphasizing active processing:
■ Central Executive: Oversees and integrates information.
■ Phonological Loop: Deals with verbal/auditory info.
■ Visuospatial Sketchpad: Handles visual/spatial info.
■ Episodic Buffer: Combines information into a coherent
sequence.
■ Levels of Processing Model (Craik and Lockhart):
■ Suggests memory retention depends on depth of processing:
■ Shallow Processing: Focus on surface features (e.g.,
appearance).
■ Deep Processing: Focus on meaning and associations,
leading to better retention.
■ Neurobiological Mechanisms:
■ Long-Term Potentiation (LTP): Strengthening of synaptic
connections through repeated activation.
■ Neurotransmitters: E.g., glutamate plays a key role in memory
formation.
■ Hippocampus: Critical for encoding episodic and spatial
memories.
■ Hebbian Theory:
■ "Neurons that fire together, wire together."
■ Learning and memory involve strengthening synaptic connections
between neurons.
● What brain regions are involved in memory processing?
Key Brain Regions in Memory Processing
○ 1. Hippocampus
■ Role: Essential for encoding and consolidating new declarative (explicit)
memories, including episodic (personal experiences) and semantic (facts)
memories.
■ Location: Medial temporal lobe.
■ Function:
■ Acts as a hub for binding information from different cortical areas
into cohesive memories.
■ Plays a role in spatial memory and navigation.
○ 2. Amygdala
■ Role: Processes emotional aspects of memory, especially fear and
reward-related memories.
■ Location: Close to the hippocampus in the temporal lobe.
■ Function: Enhances memory retention for emotionally charged events by
interacting with the hippocampus.
○ 3. Prefrontal Cortex
■ Role: Involved in working memory, decision-making, and attention.
■ Location: Front of the brain, just behind the forehead.
■ Function:
■ Central executive function in working memory (e.g., organizing,
prioritizing).
■ Retrieval and use of stored information for problem-solving and
planning.
○ 4. Cerebellum
■ Role: Important for procedural (implicit) memory and motor learning.
■ Location: Base of the brain, beneath the occipital lobe.
■ Function: Stores memories of motor skills, such as riding a bike or
playing an instrument.
○ 5. Basal Ganglia
■ Role: Supports procedural and habit formation memory.
■ Location: Deep in the brain, near the thalamus.
■ Function: Works with the cerebellum and motor areas for skill learning
and routine behaviors.
○ 6. Thalamus
■ Role: Acts as a relay station for sensory information and regulates
attention, contributing to encoding and retrieval.
■ Location: Center of the brain.
■ Function: Facilitates the flow of sensory input to relevant memory
systems.
○ 7. Parietal Lobe
■ Role: Involved in processing and integrating sensory information.
■ Function: Helps reconstruct memories, particularly visuospatial and
sensory aspects.
○ 8. Temporal Lobe
■ Role: Houses the hippocampus and amygdala; key for declarative
memory.
■ Function: Processes auditory information and contributes to memory
formation and storage.
○ 9. Occipital Lobe
■ Role: Supports visual memory processing.
■ Function: Integrates visual information into memory, such as recognizing
familiar faces or places.
○ Neurobiological Mechanisms in Memory
■ Long-Term Potentiation (LTP): Strengthens synaptic connections,
primarily in the hippocampus and cortex.
■ Neurotransmitters:
■ Glutamate: Critical for synaptic plasticity.
■ Dopamine: Modulates reward-related memory processes.
■ Acetylcholine: Essential for attention and encoding.
● How do we study and measure/test memory?
○ 1. Experimental Behavioral Tests
These involve tasks designed to assess memory performance under controlled
conditions.
■ Short-Term and Working Memory Tests
■ Digit Span Task:
■ Participants repeat a sequence of numbers in the same
(forward) or reverse (backward) order.
■ Measures short-term memory capacity and working
memory.
■ N-back Task:
■ Participants identify when a stimulus matches one
presented n steps earlier.
■ Assesses working memory and updating capabilities.
■ Corsi Block-Tapping Test:
■ Participants replicate a sequence of spatial locations
tapped by the experimenter.
■ Evaluates visuospatial short-term memory.
■ Long-Term Memory Tests
■ Recall Tests:
■ Free Recall: Participants recall as many items as possible
from a previously studied list.
■ Cued Recall: Participants receive hints or cues to aid
memory retrieval.
■ Recognition Tests:
■ Participants identify previously studied items from a list of
options, including distractors.
■ Paired-Associate Learning:
■ Participants memorize word pairs and later recall one word
when the other is presented.
■ Prospective Memory Tasks:
■ Assess memory for future intentions, such as remembering
to perform an action at a specific time.
■ Implicit Memory Tests
■ Word Fragment Completion:
■ Participants fill in blanks in fragmented words, often
influenced by previously seen stimuli (priming).
■ Mirror Drawing Task:
■ Measures procedural memory by asking participants to
trace an image while only viewing it in a mirror.
○ 2. Clinical and Neuropsychological Tests
Used to diagnose memory impairments, such as in amnesia, Alzheimer’s
disease, or traumatic brain injuries.
■ Wechsler Memory Scale (WMS):
 ■ Assesses various aspects of memory, including immediate and
delayed recall, visual memory, and auditory memory.
■ Rey Auditory Verbal Learning Test (RAVLT):
■ Measures verbal learning and memory, including immediate recall,
delayed recall, and recognition.
■ Mini-Mental State Examination (MMSE):
■ Screens for cognitive decline, including memory deficits.
○ 3. Neuroimaging Techniques
These methods allow researchers to observe memory-related brain activity and
identify the neural correlates of memory.
■ fMRI (Functional Magnetic Resonance Imaging):
■ Tracks blood flow changes in the brain during memory tasks to
identify active regions (e.g., hippocampus, prefrontal cortex).
■ EEG (Electroencephalography):
■ Records electrical activity to study brain processes underlying
memory encoding and retrieval.
■ PET (Positron Emission Tomography):
■ Detects metabolic activity in memory-related areas during
cognitive tasks.
■ Structural MRI:
■ Examines structural changes in brain regions like the
hippocampus, often in cases of neurodegeneration.
○ 4. Animal Studies
Animal models are used to explore the biological basis of memory.
■ Morris Water Maze:
■ Assesses spatial memory by training rodents to locate a hidden
platform in a water pool.
■ Fear Conditioning:
■ Evaluates associative memory by pairing a stimulus (e.g., tone)
with an aversive event (e.g., shock).
■ Electrophysiology:
■ Records neuronal activity during memory tasks to study
mechanisms like long-term potentiation (LTP).
○ 5. Computational and AI-Based Approaches
■ Cognitive Modeling:
■ Simulates memory processes using computer algorithms to
understand underlying mechanisms.
■ Big Data Analysis:
■ Analyzes patterns in memory performance across large datasets
to identify factors influencing memory.
○ 6. Self-Report and Observational Tools
■ Questionnaires:
■ E.g., Prospective and Retrospective Memory Questionnaire
(PRMQ) to assess everyday memory performance.
 ■ Observational Studies:
■ Evaluate real-world memory use, such as remembering
appointments or daily routines.
● What neurocognitive disorders affect short-term memory?
○ 1. Alzheimer’s Disease (AD)
■ Impact: Early-stage Alzheimer’s typically affects short-term memory first.
Patients struggle to retain new information but may recall older memories.
■ Affected Areas: Hippocampus, entorhinal cortex, and frontal lobes.
■ Mechanisms:
■ Neurofibrillary tangles and beta-amyloid plaques damage neurons.
■ Impaired acetylcholine signaling disrupts STM processing.
○ 2. Traumatic Brain Injury (TBI)
■ Impact: STM deficits are common after TBI, particularly in cases
involving frontal or temporal lobe damage.
■ Affected Areas: Prefrontal cortex, which governs working memory and
attention, and the hippocampus.
■ Mechanisms: Axonal injury, inflammation, and disruptions in neural
communication.
○ 3. Stroke
■ Impact: Stroke-induced damage to brain regions involved in STM,
particularly in the left hemisphere, can cause significant STM
impairments.
■ Affected Areas: Frontal and parietal lobes, thalamus.
■ Mechanisms: Ischemia (lack of blood flow) damages regions supporting
STM and working memory functions.
○ 4. Korsakoff Syndrome (Alcohol-Related Memory Disorder)
■ Impact: Caused by chronic alcohol misuse and thiamine (vitamin B1)
deficiency, it often results in profound STM deficits.
■ Affected Areas: Thalamus and mammillary bodies, connected to
memory circuits.
■ Mechanisms: Thiamine deficiency disrupts neuronal energy metabolism,
impairing STM.
○ 5. Schizophrenia (psychotic disorder)*
■ Impact: Working memory (a component of STM) is severely impaired,
affecting the ability to process and manipulate information.
■ Affected Areas: Prefrontal cortex, specifically the dorsolateral prefrontal
cortex (DLPFC).
■ Mechanisms: Dysfunction in dopamine signaling and synaptic
connectivity.
○ 6. Attention-Deficit/Hyperactivity Disorder (ADHD) (neurodevelopmental
disorder)*
■ Impact: Individuals with ADHD often experience deficits in working
memory, affecting their ability to hold and manipulate short-term
information.
 ■ Affected Areas: Prefrontal cortex and its connections to the basal
ganglia.
■ Mechanisms: Dysregulated dopamine and norepinephrine systems.
○ 7. Mild Cognitive Impairment (MCI)
■ Impact: Often considered a precursor to Alzheimer’s or other dementias,
MCI frequently includes STM difficulties.
■ Affected Areas: Hippocampus and frontal lobes.
■ Mechanisms: Early neurodegeneration affecting encoding and retrieval
processes.
○ 8. Frontotemporal Dementia (FTD)
■ Impact: STM impairments arise from degeneration in the frontal and
temporal lobes, though long-term memory may initially remain intact.
■ Affected Areas: Prefrontal cortex and anterior temporal lobes.
■ Mechanisms: Neuronal loss and abnormal protein accumulations (e.g.,
tau or TDP-43).
○ 9. Parkinson’s Disease (PD)
■ Impact: STM deficits, particularly in working memory, are common due to
impaired executive function.
■ Affected Areas: Basal ganglia, prefrontal cortex, and dopamine
pathways.
■ Mechanisms: Dopamine depletion affects the circuitry needed for STM
and cognitive flexibility.
○ 10. Anxiety and Depression (anxiety disorder)*
■ Impact: Both disorders can impair STM, often due to reduced focus,
attention, and mental energy.
■ Affected Areas: Prefrontal cortex and hippocampus (reduced volume in
chronic depression).
■ Mechanisms: Dysregulation of stress hormones (e.g., cortisol) and
neurotransmitter imbalances.
○ 11. Post-Traumatic Stress Disorder (PTSD) (anxiety disorder)*
■ Impact: STM deficits in PTSD result from heightened arousal and
intrusive memories overwhelming cognitive resources.
■ Affected Areas: Hippocampus and prefrontal cortex (reduced activity).
■ Mechanisms: Chronic stress and hyperactivity in the amygdala disrupt
STM.
○ 12. Multiple Sclerosis (MS)
■ Impact: Cognitive symptoms, including STM deficits, occur due to
demyelination affecting neural connectivity.
■ Affected Areas: Frontal lobes and hippocampus.
■ Mechanisms: Inflammation and lesions impair signal transmission
necessary for STM.
○ 13. Epilepsy
■ Impact: Seizures, particularly in the temporal lobe, can cause episodic
STM deficits.
 ■ Affected Areas: Hippocampus and surrounding temporal lobe structures.
■ Mechanisms: Repeated seizure activity damages neurons involved in
STM encoding and retrieval.
○ 14. Aging (Normal Cognitive Decline)
■ Impact: While normal aging affects STM mildly, older adults may
experience slower processing and reduced capacity.
■ Affected Areas: Prefrontal cortex and hippocampus.
■ Mechanisms: Reduced synaptic plasticity, slower neural transmission,
and changes in neurotransmitter levels.
○ 15. Hypoxia/Anoxia
■ Impact: Oxygen deprivation, as in drowning or cardiac arrest, can result
in STM impairments due to damage to memory-related regions.
■ Affected Areas: Hippocampus and prefrontal cortex.
■ Mechanisms: Neuronal death caused by lack of oxygen supply.

Memory (LTM)
● What is long term memory?
Long-term memory (LTM) is a type of memory responsible for storing information over
extended periods, ranging from minutes to a lifetime. It allows us to retain knowledge,
experiences, skills, and events that shape our understanding of the world and ourselves.
○ Duration:
■ Long-term memory can last from hours to decades, sometimes persisting
for an entire lifetime.
○ Capacity:
■ The capacity of LTM is virtually limitless. Unlike short-term memory, which
holds a limited amount of information, LTM can store vast quantities of
data.
○ Encoding:
■ Information is typically encoded in LTM through semantic processing
(understanding meaning), but other forms like visual or auditory encoding
can also contribute.
○ Consolidation:
■ The process by which short-term memories are transformed into
long-term memories. This often happens during sleep when the brain
reorganizes and stabilizes memories.
○ Retrieval:
■ Accessing stored information in LTM can be conscious (explicit recall) or
unconscious (implicit retrieval).
○ Forgetting:
■ Although LTM is relatively stable, forgetting can occur due to interference,
decay, or retrieval failure. However, some forgotten memories can be
recovered with the right cues.
○ Types of Long-Term Memory:
■ Explicit (Declarative) Memory: Conscious recall of facts and
experiences.
■ Episodic Memory: Personal experiences and events.
■ Semantic Memory: General knowledge and facts.
■ Implicit (Non-declarative) Memory: Unconscious memory of skills and
procedures.
■ Procedural Memory: Skills and habits, such as riding a bike.
■ Priming: Enhanced ability to recognize stimuli due to previous
exposure.
■ Classical Conditioning: Associating stimuli with responses.
○ What are different types of long term memory
Long-term memory (LTM) is divided into explicit (declarative) and implicit
(non-declarative) types, each with subcategories. Here's a breakdown:
■ 1. Explicit (Declarative) Memory
This involves memories that can be consciously recalled, like facts and
events.
a. Episodic Memory
■ What it stores: Personal experiences and events.
■ Examples: Your first day of school, a recent vacation.
■ Key Feature: Time and context are crucial. It often involves
mental "time travel" to re-experience the event.
■ b. Semantic Memory
■ What it stores: General knowledge and facts about the world.
■ Examples: Knowing that Paris is the capital of France,
understanding what a dog is.
■ Key Feature: Independent of personal experiences; focuses on
"what" rather than "when" or "where."
■ 2. Implicit (Non-Declarative) Memory
This involves memories that are not consciously recalled but influence
behavior and skills.
a. Procedural Memory
■ What it stores: Skills and habits.
■ Examples: Riding a bike, typing on a keyboard, playing an
instrument.
■ Key Feature: Muscle memory; it becomes automatic over time
with practice.
■ b. Priming
■ What it stores: Previous exposure to a stimulus influences
response to similar stimuli.
■ Examples: If you’ve recently seen the word “tree,” you’re quicker
to recognize related words like “leaf.”
■ Key Feature: Occurs without conscious awareness.
 ■ c. Classical Conditioning
■ What it stores: Associations between stimuli and responses.
■ Examples: Feeling anxious when hearing the sound of a dentist’s
drill due to past experiences.
■ Key Feature: Learning through association (Pavlov’s dog
salivating at the sound of a bell).
■ d. Emotional Conditioning
■ What it stores: Emotional responses tied to specific stimuli.
■ Examples: Feeling happy when you hear a favorite song from
your childhood.
■ Key Feature: A subset of implicit memory where emotional states
are triggered by past experiences.
■ 3. Prospective Memory (Crosses Categories)
■ What it stores: Remembering to perform actions in the future.
■ Examples: Remembering to take your medication, attend a
meeting.
■ Key Feature: It can rely on both explicit (you consciously
remember) and implicit cues (habitual triggers).
● What brain regions are involved in long term memory?
○ 1. Hippocampus
■ Function: Critical for the formation and consolidation of explicit
(declarative) memories, including both episodic and semantic memories.
■ Role in Memory:
■ Converts short-term memories into long-term memories.
■ Helps retrieve memories, especially recent ones.
■ Spatial memory (e.g., navigating environments).
■ Damage Effect: Can cause anterograde amnesia (inability to form new
long-term memories).
○ 2. Amygdala
■ Function: Plays a crucial role in emotional memories.
■ Role in Memory:
■ Enhances the encoding and storage of emotionally charged
memories.
■ Involved in fear conditioning and emotional responses to stimuli.
■ Damage Effect: Impaired emotional memory, especially fear-related
memories.
○ 3. Prefrontal Cortex
■ Function: Involved in the retrieval and organization of long-term
memories, particularly explicit ones.
■ Role in Memory:
■ Responsible for working memory and strategic recall.
■ Helps in decision-making and planning by using past experiences.
■ Damage Effect: Impairs the ability to retrieve and use memories
effectively, affecting problem-solving and planning.
 ○ 4. Cerebellum
■ Function: Important for procedural memory and motor learning.
■ Role in Memory:
■ Coordinates smooth execution of learned motor skills (e.g., riding
a bike, playing a musical instrument).
■ Involved in conditioned reflexes.
■ Damage Effect: Disrupts fine motor skill learning and execution.
○ 5. Basal Ganglia
■ Function: Works closely with the cerebellum for procedural memory and
habit formation.
■ Role in Memory:
■ Helps in learning routines and habits.
■ Plays a role in skill acquisition and automated behaviors.
■ Damage Effect: Difficulty in learning new motor skills or developing
habits.
○ 6. Thalamus
■ Function: Acts as a relay station for sensory and motor signals;
contributes to memory processing.
■ Role in Memory:
■ Plays a role in the retrieval of episodic memories.
■ Involved in regulating attention, which is critical for memory
encoding.
■ Damage Effect: Can lead to memory loss and problems with attention.
○ 7. Parietal Lobe
■ Function: Involved in the retrieval of spatial and sensory-related
memories.
■ Role in Memory:
■ Important for working memory related to spatial tasks.
■ Helps integrate sensory information into memory.
■ Damage Effect: Impairment in spatial awareness and memory.
○ 8. Temporal Lobes (including the Medial Temporal Lobe)
■ Function: Essential for the storage and retrieval of declarative memories.
■ Role in Memory:
■ Houses the hippocampus and amygdala.
■ Processes auditory and language-related memories.
■ Damage Effect: Can lead to retrograde amnesia (loss of previously
formed memories).
○ 9. Visual Cortex (Occipital Lobe)
■ Function: Involved in visual memory.
■ Role in Memory:
■ Stores visual information and contributes to recognition of faces,
objects, and scenes.
■ Damage Effect: Difficulty in recalling or recognizing visual information.
●
 Region Type of Memory Function

Hippocampus Declarative (episodic, Memory consolidation, retrieval

semantic)

Amygdala Emotional, fear conditioning Emotional memory encoding

Prefrontal Cortex Declarative, working memory Strategic recall, decision-making

Cerebellum Procedural, motor learning Skill execution, motor memory

Basal Ganglia Procedural, habits Routine behaviors, skill learning

Thalamus Episodic, attention regulation Memory retrieval, sensory relay

Parietal Lobe Spatial memory Sensory integration, spatial tasks

Temporal Lobe Declarative (episodic, Auditory/language memory,

semantic) storage

Visual Cortex Visual memory Visual recognition and recall

●
What is neuroplasticity?
Neuroplasticity, also known as brain plasticity, refers to the brain's remarkable ability
to adapt, reorganize, and form new neural connections throughout life. This capability
allows the brain to respond to learning, experience, injury, and environmental changes.
○ Key Features of Neuroplasticity
■ Adaptability
■ The brain can change in response to new experiences or stimuli.
This includes learning new skills, acquiring knowledge, or adapting
to sensory or motor deficits.
■ Reorganization
■ When certain areas of the brain are damaged (e.g., from a stroke),
other regions can take over their functions, leading to recovery.
■ Lifelong Process
■ While neuroplasticity is more pronounced in childhood, it
continues throughout adulthood, although the rate of change may
decrease with age.
○ Types of Neuroplasticity
■ Structural Plasticity
■ Refers to changes in the physical structure of the brain.
■ Example: Growth of new dendrites or synapses after learning or
practice.
■ Functional Plasticity
 ■Refers to the brain's ability to shift functions from damaged areas
to undamaged ones.
■ Example: Recovery of language abilities after a stroke, where
another part of the brain compensates for the damaged language
center.
○ Mechanisms of Neuroplasticity
■ Synaptic Plasticity
■ Changes in the strength of connections (synapses) between
neurons.
■ Long-Term Potentiation (LTP): Strengthening of synapses,
essential for learning and memory.
1. Resting State (Baseline Communication)
■ Neurons at Rest: Neurons are at rest, and there is normal
synaptic communication. The presynaptic neuron releases
glutamate (the excitatory neurotransmitter) into the
synaptic cleft, which binds to the AMPA receptors on the
postsynaptic neuron.
■ Weak Transmission: The synapse has a certain level of
transmission, but it is not as strong as it could be. The
postsynaptic neuron is only weakly depolarized by the
activation of AMPA receptors.
■ 2. Repeated Stimulation and Co-activation (Inducing
Potentiation)
■ High-Frequency Stimulation: The presynaptic neuron
sends high-frequency action potentials (signals) to the
postsynaptic neuron in a pattern of simultaneous or closely
timed firing.
■ Glutamate Release: As a result of this stimulation,
glutamate is released from the presynaptic neuron and
binds to the AMPA receptors (already on the postsynaptic
neuron), causing ion channels to open and allowing
sodium ions (Na⁺) to flow into the postsynaptic cell.
■ Postsynaptic Depolarization: The influx of Na⁺ causes
depolarization (a change in the electrical charge) of the
postsynaptic neuron.
■ 3. Activation of NMDA Receptors (Key Step in LTP)
■ NMDA Receptors Activation: With the postsynaptic
neuron depolarized, the NMDA receptors (a type of
glutamate receptor) become active. Normally, these
receptors are blocked by magnesium (Mg²⁺) ions.
■ Magnesium Block Removal: Depolarization of the
postsynaptic membrane causes the magnesium block to
 be expelled from the NMDA receptor channels, allowing
calcium ions (Ca²⁺) to enter the postsynaptic neuron.
■ 4. Calcium Influx and Intracellular Signaling
■ Calcium Influx: The entry of Ca²⁺ ions into the
postsynaptic neuron is crucial. Calcium acts as a signaling
molecule, initiating a cascade of intracellular events.
■ Activation of Signaling Pathways: The calcium influx
activates various protein kinases (enzymes that add
phosphate groups to other proteins), such as CaMKII
(Calcium/Calmodulin-dependent Protein Kinase II) and
PKC (Protein Kinase C).
■ These kinases trigger multiple cellular responses
that lead to the strengthening of the synapse.
■ 5. Synaptic Strengthening
■ Increase in AMPA Receptors: As a result of the signaling
cascade, more AMPA receptors are inserted into the
postsynaptic membrane, which increases the postsynaptic
neuron's sensitivity to glutamate.
■ Increased Neurotransmitter Release: The presynaptic
neuron may also increase the amount of glutamate it
releases, making the signal even stronger.
■ 6. Long-Term Structural Changes
■ Protein Synthesis: In the longer term, the signaling
pathways lead to changes in gene expression in the
postsynaptic neuron, which results in the synthesis of new
proteins that help maintain the potentiation.
■ Growth of Dendritic Spines: The structural changes also
include the growth of new dendritic spines (small
protrusions on the postsynaptic neuron), which enhance
the surface area for synaptic connections and further
increase synaptic strength.
■ 7. Maintenance and Stabilization of Potentiation
■ Persistent Potentiation: Over time, these changes lead to
a long-lasting increase in synaptic strength. The synaptic
connection remains potentiated, meaning future signals
are transmitted more easily.
■ Memory Formation: This strengthened synaptic
communication is thought to be the cellular basis for
learning and memory formation, as it allows neural circuits
to fire more efficiently and form more stable networks.
■ Long-Term Depression (LTD): Weakening of synapses,
important for forgetting or refining neural networks
■
 Feature Early Phase (E-LTP) Late Phase (L-LTP)

Duration Minutes to hours Hours to days (or

longer)

Stimulation Single burst of Repeated or prolonged

Requirement high-frequency stimulation stimulation

Protein No Yes
Synthesis

Dependence on CaMKII, PKC PKA, CREB

Kinases

Structural Minimal Synaptic remodeling,

Changes new synapses

■
Neurogenesis
■ The generation of new neurons, primarily in the hippocampus.
■ Plays a role in memory and learning.
■ Axonal Sprouting
■ Undamaged neurons grow new axons to re-establish connections
with areas that have lost their input due to injury.
■ Pruning
■ Elimination of unused or weak synaptic connections, enhancing
the efficiency of neural networks.
○ Examples of Neuroplasticity
■ Learning and Skill Development
■ Example: Musicians often show increased gray matter volume in
areas related to motor control and auditory processing.
■ Mechanism: Repeated practice strengthens the neural pathways
associated with the skill.
■ Recovery from Brain Injury
■ Example: Stroke survivors often regain lost abilities through
therapy that promotes neural reorganization.
■ Mechanism: Undamaged areas of the brain compensate for the
lost functions.
■ Sensory Substitution
■ Example: In people who are blind, the visual cortex can be
repurposed to process auditory or tactile information, enhancing
these senses.
■ Mechanism: Functional reorganization in response to sensory
deprivation.
○ Factors Influencing Neuroplasticity
 ■ Age
■ Neuroplasticity is strongest during childhood but persists, albeit at
a slower rate, throughout life.
■ Experience and Practice
■ Repeated exposure to new skills or environments enhances
plasticity.
■ Sleep
■ Crucial for memory consolidation and neural reorganization.
■ Physical Exercise
■ Promotes neurogenesis and synaptic plasticity, particularly in the
hippocampus.
■ Nutrition
■ A diet rich in omega-3 fatty acids, antioxidants, and essential
nutrients supports brain health and plasticity.
■ Stress and Mental Health
■ Chronic stress can impair neuroplasticity by reducing
neurogenesis and weakening synaptic connections, particularly in
the hippocampus.
■ Conversely, mindfulness and therapy can promote positive neural
changes.
○ Clinical Relevance of Neuroplasticity
■ Rehabilitation
■ Stroke Recovery: Neuroplasticity enables relearning of motor
skills and language through therapy.
■ Brain Injury: Allows patients to recover lost functions or adapt to
deficits.
■ Mental Health Treatment
■ Neuroplasticity plays a role in the efficacy of treatments for
conditions like depression, anxiety, and PTSD.
■ Cognitive-behavioral therapy (CBT) and antidepressants can
foster positive neural changes.
■ Learning Disabilities
■ Targeted interventions can leverage neuroplasticity to improve
learning outcomes in individuals with dyslexia or ADHD.
■ Neurodegenerative Disorders
■ Efforts to enhance neuroplasticity may slow cognitive decline in
conditions like Alzheimer’s or Parkinson’s disease.
○ Key Takeaways
■ Neuroplasticity is the brain's ability to adapt and reorganize itself.
■ It underpins learning, memory, and recovery from injury.
■ Understanding and leveraging neuroplasticity has profound implications
for education, rehabilitation, and mental health.
○ What is long term potentiation?
Long-Term Potentiation (LTP) is a process by which synaptic connections
between neurons become stronger with repeated activation. It is a key
mechanism underlying learning and memory formation in the brain.
■ Key Characteristics of LTP
■ Synaptic Strengthening
■ When two neurons are repeatedly activated together, the
connection (synapse) between them becomes stronger.
This makes future communication more efficient.
■ Long-Lasting
■ Once established, LTP can persist for hours, days, or even
longer, providing a cellular basis for long-term memory.
■ Activity-Dependent
■ LTP requires repeated or intense stimulation of synapses,
often described as "neurons that fire together, wire
together."
■ Where Does LTP Occur?
LTP is most commonly studied in the hippocampus, a brain region
critical for learning and memory. Specifically, it occurs at synapses in:
■ CA1 and CA3 regions of the hippocampus.
■ Dentate gyrus.
■ However, LTP can also occur in other brain regions, such as the cortex
and amygdala, supporting different types of memory.
■ How LTP Works: Mechanisms
■ Induction Phase (Initiating LTP)
■ High-frequency stimulation of a presynaptic neuron leads
to the release of glutamate, a key excitatory
neurotransmitter.
■ Glutamate binds to AMPA receptors, causing an influx of
sodium ions (Na⁺) and depolarizing the postsynaptic
neuron.
■ Once sufficiently depolarized, NMDA receptors (which are
initially blocked by magnesium ions, Mg²⁺) are activated,
allowing calcium ions (Ca²⁺) to enter the postsynaptic
neuron.
■ Expression Phase (Strengthening Synapse)
■ The influx of Ca²⁺ triggers a cascade of intracellular
signaling, leading to the insertion of more AMPA
receptors into the postsynaptic membrane.
■ This increases the postsynaptic neuron’s sensitivity to
future glutamate release.
■ Maintenance Phase (Sustaining LTP)
■ Structural changes occur, such as the growth of new
synaptic connections or dendritic spines.
■ Long-term protein synthesis is required to stabilize these
changes.
 ■ Role of LTP in Memory
■ Encoding: LTP enhances the synaptic connections necessary for
encoding new information.
■ Storage: Helps stabilize memory traces over time.
■ Retrieval: Strengthened synapses facilitate the recall of stored
information.
■ LTP is especially important for spatial memory and episodic memory,
as demonstrated in studies involving the hippocampus.
■ Experimental Evidence for LTP
■ Bliss and Lømo (1973)
■ The phenomenon of LTP was first discovered in the
hippocampus of rabbits. Repeated electrical stimulation of
certain synapses led to prolonged enhancement of
synaptic strength.
■ Knockout Mice Studies
■ Mice genetically engineered to lack NMDA receptors in the
hippocampus show impaired LTP and memory deficits,
highlighting the critical role of NMDA receptors.
■ Behavioral Correlation
■ Improved LTP has been linked to better performance in
memory tasks, such as navigating a maze.
■ Clinical and Practical Relevance of LTP
■ Cognitive Enhancement
■ Understanding LTP may lead to therapies aimed at
enhancing memory and learning in healthy individuals.
■ Memory Disorders
■ Impaired LTP is associated with conditions like
Alzheimer’s disease, where synaptic weakening leads to
memory loss.
■ Research into boosting LTP may offer strategies to combat
cognitive decline.
■ Neuroplasticity
■ LTP underpins the brain’s ability to adapt through
experience, training, or recovery from injury.
■ Key Takeaways
■ LTP is a fundamental mechanism for strengthening synaptic
connections, forming the basis of long-term memory and learning.
■ It primarily involves the hippocampus and depends on the activity
of AMPA and NMDA receptors.
■ LTP offers crucial insights into both normal cognitive function and
the treatment of memory-related disorders.
● Ways to study long term memory
○ 1. Experimental Techniques in Psychology
Researchers design experiments to test specific aspects of memory, such as
 recall, recognition, and forgetting.
a. Free Recall and Cued Recall Tests
■ Purpose: Examine how well participants remember information without
prompts (free recall) or with hints (cued recall).
■ Example: Participants are asked to recall a list of words after studying
them. In cued recall, they might be given the first letter of each word.
○ b. Recognition Tests
■ Purpose: Measure the ability to recognize previously learned information.
■ Example: Participants study a list of words and later identify them from a
new list that includes distractors.
○ c. Paired-Associate Learning
■ Purpose: Test associative memory by pairing items together.
■ Example: Participants learn word pairs (e.g., "dog - tree") and are later
asked to recall the second word when given the first.
○ d. Repetition and Spacing Effects
■ Purpose: Study how repeated exposure and spacing between study
sessions affect memory retention.
■ Example: Comparing retention after massed practice (cramming) versus
spaced practice (distributed learning).
○ 2. Neuroimaging Techniques
These methods allow researchers to observe brain activity related to memory in
real time.
a. Functional Magnetic Resonance Imaging (fMRI)
■ Purpose: Identifies active brain regions during memory tasks.
■ Example: Observing hippocampal activation when participants recall
personal experiences.
○ b. Electroencephalography (EEG)
■ Purpose: Measures electrical activity in the brain, especially during
memory encoding and retrieval.
■ Example: Studying the timing of neural responses associated with
successful memory recall.
○ c. Positron Emission Tomography (PET)
■ Purpose: Tracks metabolic processes in the brain to identify areas
involved in memory.
■ Example: Analyzing glucose consumption in the hippocampus during
memory tasks.
○ 3. Behavioral Studies in Real-World Settings
Observing memory in natural environments helps researchers understand its
practical applications.
a. Diary Studies
■ Purpose: Participants keep a record of daily events, which are later used
to test episodic memory.
 ■ Example: Comparing participants’ written accounts with their recall
accuracy over time.
○ b. Prospective Memory Tasks
■ Purpose: Examine memory for future tasks.
■ Example: Participants are asked to remember to perform a task at a
specific time or when a particular event occurs.
○ 4. Clinical Case Studies
Studying individuals with memory impairments provides insights into how
different brain regions contribute to memory.
a. Amnesia Studies
■ Purpose: Investigate the effects of brain damage on memory.
■ Example: Studying patients with hippocampal damage (e.g., H.M.) to
understand declarative memory deficits.
○ b. Neurodegenerative Disorders
■ Purpose: Explore memory decline in conditions like Alzheimer’s disease.
■ Example: Examining how semantic and episodic memories deteriorate
over time.
○ 5. Cognitive and Computational Modeling
Researchers use mathematical and computer models to simulate memory
processes.
■ Purpose: Understand how memory systems work and predict behavior.
■ Example: Creating models that simulate how information is stored and
retrieved in the brain.
○ 6. Longitudinal Studies
■ Purpose: Examine how memory changes over time in the same group of
participants.
■ Example: Tracking memory performance in individuals across decades to
study aging effects.
○ 7. Memory Training and Intervention Studies
■ Purpose: Test strategies for improving memory.
■ Example: Evaluating the effectiveness of mnemonic devices, spaced
repetition, or physical exercise on long-term memory enhancement.
○ 8. Genetic and Pharmacological Studies
■ Purpose: Investigate biological factors influencing memory.
■ Example: Exploring the role of specific genes or testing drugs that
enhance memory performance.
○ Explain the HM case, what do the pictures show us?
It provided groundbreaking insights into the structure and function of memory,
particularly the role of the hippocampus in forming long-term memories.
■ Background of H.M.
■ Born: 1926, Connecticut, USA.
■ Condition: H.M. suffered from severe epilepsy starting in
childhood, with debilitating seizures that could not be controlled by
medication.
 ■ Surgery: At age 27 (in 1953), H.M. underwent an experimental
surgery performed by neurosurgeon William Scoville to alleviate
his seizures. The procedure involved the removal of large portions
of the medial temporal lobes, including most of the
hippocampus, amygdala, and surrounding cortical areas on both
sides of his brain.
■ Outcomes of the Surgery
■ Success: The surgery significantly reduced H.M.’s seizures.
■ Severe Memory Impairment:
■ Anterograde Amnesia: H.M. could not form new explicit
(declarative) long-term memories. He was unable to
remember events or facts learned after the surgery.
■ Partial Retrograde Amnesia: H.M. lost memories of
events from the years leading up to the surgery, but his
childhood memories remained largely intact.
■ Intact Short-Term Memory: He could retain information
for short periods (e.g., remembering a number for 20
seconds).
■ Preserved Implicit Memory: H.M. could learn new motor
skills and habits without remembering the training process
(e.g., improving at tasks like mirror drawing, a procedural
memory skill).
■ Key Insights from H.M.’s Case
■ Hippocampus Is Crucial for Long-Term Memory Formation
■ The hippocampus is essential for converting short-term
memories into long-term explicit memories (episodic and
semantic).
■ Without it, individuals cannot store new declarative
information.
■ Memory Is Not a Single Entity
■ Explicit (Declarative) Memory: Severely impaired in H.M.
after the surgery.
■ Implicit (Non-Declarative) Memory: Procedural learning
and other unconscious memory functions remained intact.
■ This finding highlighted the distinction between different
memory systems.
■ Short-Term Memory and Working Memory Operate
Independently
■ H.M. could hold information in his short-term memory but
could not transfer it into long-term storage.
■ This provided evidence that short-term memory and
long-term memory rely on different neural mechanisms.
■ Memory Consolidation
 ■ The hippocampus plays a time-limited role in consolidating
memories. Over time, consolidated memories are stored in
other brain regions, like the neocortex.
■ The Role of the Medial Temporal Lobe in Retrieval
■ H.M.’s partial retrograde amnesia suggested that recent
memories depend on the hippocampus for retrieval until
they are fully consolidated in other regions.
■ Impact of H.M.’s Case on Neuroscience and Psychology
■ Understanding Brain-Behavior Relationships
■ H.M.’s case provided direct evidence linking specific brain
regions to memory processes.
■ Development of New Theories of Memory
■ Inspired models like the multi-store model of memory
and theories of memory consolidation.
■ Foundation for Cognitive Neuroscience
■ H.M.’s case was pivotal in establishing the field of cognitive
neuroscience, which links brain function with cognitive
processes.
■ Ethical Considerations
■ Highlighted the importance of informed consent and the
ethical treatment of patients in research.
■ Applications and Modern Research
■ Memory Disorders: H.M.’s case continues to inform the
understanding of amnesia, Alzheimer’s disease, and other
memory-related conditions.
■ Neuroimaging Studies: Subsequent imaging studies on H.M.
(post-mortem) confirmed the extent of his brain damage and
provided a detailed map of the medial temporal lobe's role in
memory.
■ Rehabilitation Strategies: Insights from H.M. have led to better
approaches for helping individuals with memory impairments
develop compensatory strategies.
■ Key Takeaways
The H.M. case profoundly shaped our understanding of memory,
revealing that:
■ Memory is not a singular process but consists of multiple systems
(explicit vs. implicit).
■ The hippocampus is essential for forming new declarative
memories.
■ Different brain regions contribute to different types of memory, with
some forms (e.g., procedural) remaining intact even with
significant hippocampal damage.
● Methods to train/improve (the encoding, storage, retrieval of) long term memory
○ 1. Improving Encoding
Encoding is the process of transforming sensory input into a format that can be
stored in memory. Strong encoding increases the likelihood of successful
long-term storage and retrieval.
■ a. Use Deep Processing (Elaborative Encoding)
■ What: Focus on the meaning of information and make
connections to what you already know.
■ How: Relate new information to personal experiences, create
examples, or explain it to someone else.
■ Example: When learning a new psychology concept, link it to
real-world scenarios or case studies.
■ b. Use Mnemonic Devices
■ What: Techniques that aid memory through patterns or
associations.
■ How:
■ Acronyms: e.g., HOMES for the Great Lakes (Huron,
Ontario, Michigan, Erie, Superior).
■ Method of Loci: Associate information with specific
locations in a mental "memory palace."
■ Peg System: Use visual imagery and pre-memorized lists
(e.g., "one is a bun").
■ c. Chunking
■ What: Break down large amounts of information into smaller,
manageable chunks.
■ How: Instead of memorizing a long sequence of numbers, group
them into smaller sets (e.g., 199819941997 → 1998, 1994, 1997).
■ d. Multisensory Learning
■ What: Use multiple senses to enhance encoding.
■ How: Combine visual aids, auditory inputs (e.g., repeating aloud),
and kinesthetic activities (e.g., writing notes by hand).
■ e. Attention Management
■ What: Focus fully on the material.
■ How: Minimize distractions (e.g., phone, noise) and study in a
quiet, organized space.
○ 2. Enhancing Storage
Storage refers to the process of maintaining information in long-term memory
over time.
■ a. Spaced Repetition
■ What: Review material at gradually increasing intervals.
■ How: Use tools like Anki or Quizlet to schedule reviews based on
your forgetting curve.
■ Why: Helps transfer knowledge from short-term to long-term
memory.
■ b. Sleep and Memory Consolidation
 ■ What: Sleep plays a crucial role in consolidating memories.
■ How: Aim for 7–9 hours of sleep per night and take short naps
after intense study sessions.
■ Why: The hippocampus reorganizes and integrates new
information into long-term memory during sleep.
■ c. Healthy Lifestyle
■ What: Good physical and mental health improve memory storage.
■ How:
■ Exercise regularly to boost brain plasticity.
■ Maintain a balanced diet with memory-enhancing nutrients
(e.g., Omega-3s, antioxidants).
○ 3. Improving Retrieval
Retrieval is the process of accessing stored information when needed. Strong
retrieval skills depend on how well information was encoded and stored.
■ a. Practice Retrieval (Active Recall)
■ What: Regularly test yourself on the material.
■ How: Use flashcards or quiz questions. Try to recall information
without looking at your notes.
■ Why: Strengthens neural pathways associated with the memory.
■ b. Contextual Cues
■ What: Study in an environment similar to the one where you’ll
need to recall the information.
■ How: If preparing for an exam, simulate exam conditions.
■ Why: Context-dependent memory helps retrieval in similar
contexts.
■ c. State-Dependent Learning
■ What: Recall is better if your physical or emotional state matches
the state you were in during encoding.
■ How: If you study while slightly energized (e.g., after moderate
exercise), try to replicate that state during retrieval.
■ d. Use Retrieval Cues
■ What: Associate specific cues with the information you want to
recall.
■ How: Use keyword associations, images, or even smells linked to
the material.
■ e. Overlearning
■ What: Continue practicing even after you’ve mastered the
material.
■ How: Review content multiple times to strengthen memory traces.
■ Why: Overlearning increases retrieval speed and accuracy.
○ 4. General Strategies for Overall Memory Improvement
■ a. Mindfulness and Meditation
■ What: Practices that enhance focus and reduce stress.
 ■ How: Daily meditation can improve working memory, leading to
better long-term memory storage.
■ b. Physical Exercise
■ What: Boosts blood flow and neurogenesis (growth of new brain
cells).
■ How: Incorporate aerobic exercises like running or swimming.
■ Why: Improves brain plasticity, especially in the hippocampus.
■ c. Brain Training Games
■ What: Games designed to improve cognitive functions.
■ How: Use apps like Lumosity or Peak to challenge your memory,
attention, and problem-solving skills.
■ d. Visualization Techniques
■ What: Create vivid mental images of the information.
■ How: When studying history, visualize the events as scenes in a
movie.
■ e. Teaching Others
■ What: Explaining concepts to others helps solidify your
understanding.
■ How: Teach a friend or pretend you’re giving a lecture.
● What is memory consolidation?
Memory consolidation is the process by which temporary, fragile memories are
transformed into more stable, long-lasting ones. This process is essential for transferring
information from short-term memory or working memory to long-term memory.
Consolidation helps memories resist interference and decay, making them accessible
over extended periods.

○ Types of Memory Consolidation

■ Synaptic Consolidation (Short-Term Process)
■ Occurs within minutes to hours after learning.
■ Involves changes in the strength of synaptic connections between
neurons.
■ Relies on processes like long-term potentiation (LTP), which
strengthens synapses through repeated activation.
■ Takes place in the hippocampus and other regions involved in
initial memory formation.
■ Systems Consolidation (Long-Term Process)
■ Occurs over days, weeks, or even years.
■ Involves the gradual transfer of memories from the hippocampus
to the neocortex for long-term storage.
■ Episodic memories, for instance, become less dependent on the
hippocampus over time and are stored more broadly across the
brain.
○ Phases of Memory Consolidation
■ Encoding Phase
 ■ Initial processing of new information.
■ Involves the hippocampus and related structures for organizing
and linking information.
■ Early Consolidation
■ Happens shortly after learning.
■ Memories are fragile and prone to disruption.
■ Late Consolidation
■ Stabilizes memories over time.
■ Involves reorganization of memory traces within the brain.
○ Factors Influencing Memory Consolidation
■ Sleep
■ One of the most critical factors for memory consolidation.
■ During sleep, especially slow-wave sleep (SWS) and REM sleep,
the brain replays and strengthens newly learned information.
■ The hippocampus and neocortex communicate during sleep to
consolidate memories.
■ Rehearsal and Practice
■ Repetition and review of information strengthen memory traces.
■ Techniques like spaced repetition enhance consolidation by
reinforcing memories at optimal intervals.
■ Emotional Arousal
■ Emotional events are often remembered better due to the role of
the amygdala in enhancing consolidation.
■ Strong emotions (e.g., fear, excitement) signal the brain to
prioritize certain memories.
■ Nutrition and Physical Health
■ Nutrients like Omega-3 fatty acids, antioxidants, and adequate
hydration support brain function.
■ Physical exercise promotes neurogenesis in the hippocampus,
aiding memory consolidation.
■ Stress
■ Moderate stress can enhance consolidation by activating the
amygdala and improving focus.
■ Chronic stress, however, impairs memory consolidation due to
high levels of cortisol, which can damage the hippocampus.
○ The Role of Reconsolidation
■ Reconsolidation occurs when a previously consolidated memory is
recalled, becomes temporarily unstable, and must be re-stabilized.
■ This process allows memories to be updated or modified with new
information.
■ Useful in therapies like trauma-focused therapy, where maladaptive
memories can be reprocessed.
○ Clinical Relevance
 ■ Amnesia: Patients with hippocampal damage (e.g., H.M.) struggle with
consolidation, particularly for declarative memories.
■ Neurodegenerative Diseases: Conditions like Alzheimer’s disease
impair the consolidation process, leading to memory loss.
■ PTSD: Strong emotional memories are overly consolidated, making them
difficult to suppress or forget.
○ Key Takeaways
■ Memory consolidation is essential for creating stable, long-term
memories.
■ It involves short-term changes at the synaptic level and long-term
reorganization across brain systems.
■ Factors like sleep, rehearsal, and emotional arousal significantly enhance
the consolidation process.
● Theories of Memory Consolidation
○ Standard Model of Memory Consolidation: This model suggests that
memories are initially dependent on the hippocampus and gradually become
independent as they are transferred to the neocortex.
○ Multiple Trace Theory: Proposes that episodic memories remain dependent on
the hippocampus even after consolidation, with multiple traces being distributed
across different brain regions.
○ Dual Process Theory: Suggests that the hippocampus and the neocortex
contribute to different types of memory (e.g., the hippocampus for episodic and
contextual memory, and the neocortex for semantic and procedural memory).
● What disorders affect long-term memory?
○ 1. Neurodegenerative Disorders
These conditions involve the progressive loss of neurons and are strongly
associated with long-term memory deficits.
■ a. Alzheimer's Disease (AD)
Effects:
■ Early stages: Impairs episodic memory (e.g., difficulty recalling
recent events).
■ Later stages: Affects semantic memory (e.g., loss of general
knowledge) and procedural memory.
■ Cause: Build-up of beta-amyloid plaques and tau tangles in the brain,
leading to neuronal death.
Affected Areas: Hippocampus (early) and neocortex (later).
■ b. Dementia (Various Types)
Effects: Decline in multiple cognitive domains, including memory,
language, and problem-solving.
Types:
■ Vascular Dementia: Memory loss due to impaired blood flow to
the brain.
■ Lewy Body Dementia: Affects memory, visual processing, and
motor control.
 ■ c. Parkinson's Disease (PD)
Effects: Memory impairment, especially in later stages.
Cause: Degeneration of dopaminergic neurons, which impacts brain
areas involved in memory and executive function.
■ d. Huntington's Disease
Effects: Gradual decline in cognitive functions, including memory.
Cause: Genetic mutation leading to brain cell death, particularly in the
basal ganglia and cerebral cortex.
○ 2. Amnestic Disorders
These disorders are characterized by significant memory loss.
■ a. Anterograde Amnesia
■ Definition: Inability to form new long-term memories after the
onset of the disorder.
■ Cause: Often due to damage to the hippocampus or surrounding
medial temporal lobe structures.
■ Example: H.M.’s case.
■ b. Retrograde Amnesia
■ Definition: Loss of pre-existing memories, often for a specific time
period.
■ Cause: Traumatic brain injury, strokes, or psychological trauma.
■ c. Korsakoff’s Syndrome
■ Effects: Severe anterograde and retrograde amnesia.
■ Cause: Thiamine (Vitamin B1) deficiency, often associated with
chronic alcoholism.
■ Affected Areas: Mammillary bodies and thalamus, which are part
of the brain's memory circuits.
○ 3. Traumatic Brain Injury (TBI)
■ Effects: Can result in both anterograde and retrograde amnesia.
■ Cause: Physical injury to the brain, such as from a car accident or a fall.
■ Severity:
■ Mild TBI (concussion): Temporary memory loss.
■ Severe TBI: Long-term or permanent memory impairment.
○ 4. Psychological Disorders
Memory impairment can also occur in the context of certain mental health
conditions.
■ a. Post-Traumatic Stress Disorder (PTSD)
■ Effects: Impairs retrieval of autobiographical memories and may
lead to fragmented or overly vivid recall of traumatic events.
■ Cause: Hyperactivity in the amygdala and reduced activity in the
prefrontal cortex.
■ b. Depression
■ Effects: Affects both episodic and semantic memory, with retrieval
being particularly impaired.
 ■ Cause: Dysregulation of neurotransmitters and reduced activity in
the prefrontal cortex and hippocampus.
■ c. Anxiety Disorders
■ Effects: Can interfere with memory retrieval, especially under
stress.
■ Cause: Overactivation of the amygdala and disruption of focus
during encoding.
○ 5. Epilepsy
■ Effects: Memory problems can arise from seizures that affect the
hippocampus or surrounding areas.
■ Types:
■ Temporal Lobe Epilepsy: Frequently associated with memory
impairments.
■ Status Epilepticus: Prolonged seizures can cause lasting
damage to memory-related regions.
○ 6. Stroke
■ Effects: Depending on the location of the stroke, long-term memory may
be affected.
■ Cause: Interruption of blood flow to memory-related brain regions (e.g.,
hippocampus, thalamus).
■ Type of Memory Loss: Can affect episodic, semantic, or procedural
memory, depending on the brain regions impacted.
○ 7. Brain Infections and Inflammation
Infections that affect the brain can lead to memory impairments.
a. Encephalitis
■ Effects: Severe cases can cause long-term memory loss.
■ Cause: Viral infections (e.g., herpes simplex virus) or autoimmune
responses leading to brain inflammation.
○ b. Meningitis
■ Effects: Can result in long-term cognitive and memory problems if the
brain is affected.
○ 8. Sleep Disorders
Chronic sleep issues disrupt the consolidation of long-term memories.
a. Sleep Apnea
■ Effects: Frequent interruptions of deep sleep impact memory
consolidation.
■ Cause: Repeated oxygen deprivation during sleep.
○ b. Insomnia
■ Effects: Reduces the quality of sleep necessary for memory processing.
○ 9. Multiple Sclerosis (MS)
■ Effects: Episodic and working memory are commonly impaired.
■ Cause: Inflammatory damage to the brain and spinal cord, disrupting
neural pathways.
 ○ 10. Substance Abuse Disorders
■ Effects: Long-term memory can be impaired, especially with prolonged
use.
■ Substances:
■ Alcohol: Can cause both short-term and long-term memory
problems, especially in chronic use (e.g., Korsakoff's Syndrome).
■ Illicit Drugs: Substances like methamphetamine or heroin can
impair brain function and memory.

Cognitive Control
● What is cognitive control?
Cognitive control, also known as executive function, refers to a set of mental processes
that allow individuals to regulate their thoughts, emotions, and behaviors to achieve
goals or respond adaptively to complex or changing environments. It plays a crucial role
in decision-making, problem-solving, and goal-directed behavior.
○ Key Components of Cognitive Control:
■ Inhibitory Control: The ability to suppress automatic or impulsive
responses to focus on goal-relevant actions.
■ Working Memory: Holding and manipulating information in mind for short
periods, essential for reasoning and guiding decision-making.
■ Cognitive Flexibility: The capacity to switch between different tasks,
perspectives, or strategies depending on changing demands.
○ Functions of Cognitive Control:
■ Attention Regulation: Focusing on relevant stimuli while ignoring
distractions.
■ Planning and Goal Setting: Developing strategies and setting steps to
achieve objectives.
■ Error Monitoring: Recognizing and correcting mistakes to improve
performance.
■ Impulse Control: Managing urges or behaviors that may be
counterproductive.
○ Importance in Daily Life:
Cognitive control is essential for complex tasks such as studying, driving, social
interactions, and adapting to new situations. It's also critical for maintaining
self-discipline and regulating emotions in challenging circumstances.
○ Role in profiling
In profiling, cognitive control plays a critical role in analyzing behavioral patterns,
interpreting evidence, and making informed judgments. Here's how cognitive
control is applied in profiling:
■ 1. Attention to Detail
 ■ Role: Profilers need to focus on subtle clues in crime scenes,
victimology, and offender behavior. Cognitive control helps them
filter out irrelevant information and prioritize critical details.
■ Example: Noticing inconsistencies in witness statements or
identifying unique aspects of an offender's modus operandi (MO).
■ 2. Inhibitory Control
■ Role: Profilers must suppress personal biases or emotional
reactions to remain objective and focus solely on the facts.
■ Example: Avoiding snap judgments about a suspect based on
stereotypes and relying on evidence-based assessments.
■ 3. Working Memory
■ Role: Working memory helps profilers hold multiple pieces of
information in mind, such as profiles of previous offenders,
psychological theories, and current case details.
■ Example: Comparing behavioral patterns across different cases to
identify links or predict future actions.
■ 4. Cognitive Flexibility
■ Role: Profilers often deal with incomplete or evolving information.
Cognitive flexibility enables them to adapt their hypotheses as new
evidence emerges.
■ Example: Revising an offender profile when new evidence
contradicts initial assumptions.
■ 5. Decision-Making and Problem-Solving
■ Role: Profilers must make high-stakes decisions, often with limited
information, such as predicting an offender's next move or
advising law enforcement on interrogation strategies.
■ Example: Prioritizing suspects based on behavioral analysis or
suggesting specific interview techniques tailored to a suspect's
psychological profile.
■ 6. Empathy and Perspective-Taking
■ Role: While empathy isn’t strictly part of cognitive control, it works
alongside it in profiling. Understanding an offender’s mindset or
motives often involves simulating their thought processes without
condoning their actions.
■ Example: Anticipating an offender’s behavior by stepping into
their psychological world.
○ In Neuroscientific Terms:
Cognitive control is associated with the prefrontal cortex, which governs
complex decision-making, impulse control, and planning. Profilers rely heavily on
these executive functions to make sense of criminal behavior, which often
deviates from societal norms.
Would you like to delve deeper into specific techniques or cases where cognitive
control is vital in profiling?
● Different models of cognitive control
Several models have been proposed to explain cognitive control, each emphasizing
different aspects of how the brain regulates behavior and decision-making. Here are
some of the key models:

1. Supervisory Attentional System (SAS)

○ Proposed by: Norman and Shallice (1986)
○ Description: The SAS regulates behavior in non-routine or novel situations
where automatic responses are insufficient. It involves conscious, deliberate
control to override habitual actions.
○ Relevance: Explains how we manage complex tasks requiring flexibility and
inhibition of automatic responses.
●
2. Conflict Monitoring Model
○ Proposed by: Botvinick et al. (2001)
○ Description: This model highlights the role of the anterior cingulate cortex
(ACC) in detecting conflicts in information processing. When conflict arises (e.g.,
when two competing responses are possible), cognitive control systems engage
to resolve it.
○ Relevance: Important for tasks involving conflicting choices or responses, such
as the Stroop task.
●
3. Dual Mechanisms of Control
○ Proposed by: Braver (2012)
○ Description: This model distinguishes between two types of control:
■ Proactive Control: Maintaining goal-relevant information actively in mind
before a challenge arises.
■ Reactive Control: Engaging control after a conflict or error is detected.
○ Relevance: Demonstrates how cognitive control can be anticipatory or
responsive depending on the context.
●
4. Task-Set Reconfiguration Model
○ Proposed by: Monsell (2003)
○ Description: Focuses on cognitive flexibility, emphasizing the brain’s ability to
switch between different task rules or goals. This model highlights the role of the
prefrontal cortex in dynamically updating task sets.
○ Relevance: Essential for multitasking and adapting to changing environments.
○ Explain the Phineas Gage case
Background:
Phineas Gage was a 25-year-old railroad construction foreman in 1848 when he
suffered a severe brain injury. A large iron rod was accidentally driven through his
skull, passing through his left cheek and out the top of his head, damaging a
significant portion of his prefrontal cortex.
 Immediate Effects:
■ Gage miraculously survived the accident and was able to walk and talk
shortly afterward.
■ However, his personality and behavior changed dramatically, which
provided early evidence of the role of the prefrontal cortex in cognitive
control.
○
Behavioral Changes:
■ Impulsivity and Poor Decision-Making:
■ Previously responsible and organized, Gage became erratic and
impulsive.
■ He made poor decisions, showing little regard for long-term
consequences.
■ Emotional Dysregulation:
■ He displayed extreme emotional outbursts and was unable to
control his temper.
■ Loss of Social Inhibition:
■ Gage behaved inappropriately in social situations, often offending
those around him.
○
Significance of the Case:
■ Prefrontal Cortex and Cognitive Control: Gage’s case provided early
evidence that the prefrontal cortex is critical for executive functions like
planning, decision-making, emotional regulation, and social behavior.
■ Neuroscience Foundations: His case laid the groundwork for
understanding how specific brain regions contribute to different aspects of
personality and behavior.
○ Modern Implications:
Today, Gage’s case is often cited in discussions about frontal lobe damage and
its impact on executive functioning, emphasizing the importance of the prefrontal
cortex in maintaining cognitive control.
Would you like to explore more on brain regions related to cognitive control or
other famous neuroscience cases?
● Which brain areas are involved in cognitive control? -> Prefrontal lobe
The prefrontal cortex (PFC) is the primary brain region involved in cognitive control,
but it works in concert with several other brain areas. Below is an overview of the
specific regions of the prefrontal cortex and their roles, along with other related brain
areas.

1. Prefrontal Cortex (PFC)

The PFC is the brain's control center for executive functions and cognitive control. It
 consists of multiple subregions:
a. Dorsolateral Prefrontal Cortex (DLPFC)
○ Role:
■ Working memory
■ Planning and decision-making
■ Maintaining goal-directed behavior
○ Example: Holding information in mind while solving a complex problem.
● b. Ventrolateral Prefrontal Cortex (VLPFC)
○ Role:
■ Inhibitory control
■ Regulating attention
○ Example: Suppressing a habitual response when it's inappropriate in a given
context.
● c. Orbitofrontal Cortex (OFC)
○ Role:
■ Decision-making based on reward and punishment
■ Emotional regulation
○ Example: Evaluating risks and rewards before making a choice.
● d. Medial Prefrontal Cortex (mPFC)
○ Role:
■ Self-referential thinking
■ Social cognition and understanding others’ perspectives
○ Example: Making judgments about your own or someone else’s behavior.
● e. Anterior Cingulate Cortex (ACC)
○ Role:
■ Conflict monitoring and error detection
■ Adapting behavior after mistakes
○ Example: Recognizing when two competing responses (e.g., stopping or going)
are both possible and choosing the correct one.
●
2. Other Brain Areas Supporting Cognitive Control
a. Basal Ganglia
○ Role: Regulates motor control, habits, and procedural learning.
○ Example: Helps shift between tasks and manage habitual responses.
● b. Parietal Cortex
○ Role: Supports attention and integrates sensory information.
○ Example: Directing focus to relevant stimuli in a crowded environment.
● c. Amygdala
○ Role: Processes emotions, particularly fear and reward.
○ Connection to PFC: The PFC modulates amygdala activity to regulate emotional
responses.
○ Example: Managing anxiety during high-stakes decision-making.
● d. Hippocampus
○ Role: Involved in memory and spatial navigation.
○ Example: Linking past experiences to current decisions.
● e. Thalamus
○ Role: Acts as a relay station for sensory and motor signals, supporting
communication between different brain regions.
○ Example: Facilitates the flow of information required for maintaining attention.
●
Summary of Functions
The prefrontal cortex and its connected networks enable core executive functions:
○ Inhibition: Stopping impulses (DLPFC, VLPFC)
○ Flexibility: Switching strategies or adapting to change (DLPFC)
○ Monitoring: Identifying errors and conflicts (ACC)
○ Emotion Regulation: Managing emotional reactions (OFC, amygdala)
● Which types of experiments or studies are used to study cognitive control
○ 1. Behavioral Tasks
These tasks are designed to assess specific components of cognitive control,
such as inhibitory control, working memory, and cognitive flexibility.
■ a. Stroop Task
■ Purpose: Measures inhibitory control and conflict resolution.
■ Design: Participants are asked to name the color of the ink in
which a word is printed, ignoring the word itself (e.g., the word
"RED" printed in blue ink).
■ Findings: Slower responses or errors when the word and ink color
conflict, indicate difficulty in inhibiting automatic reading.
■ Hypothesis
The hypothesis of the Stroop Test typically revolves around
interference in cognitive processing. Specifically, it predicts that:
When the name of a color is printed in a color different from the
word's meaning (e.g., the word "red" printed in blue ink), people
will take longer to identify the ink color and will make more errors
compared to when the word and the ink color match or when a
neutral stimulus (e.g., non-color-related words or symbols) is
used.
Key Points:
■ Congruent condition: Word meaning and ink color match
(e.g., "red" printed in red).
■ Incongruent condition: Word meaning and ink color
conflict (e.g., "red" printed in blue).
■ Neutral condition: No color word is involved, such as
random symbols or non-color words.
■ The hypothesis is based on the idea that reading words is an
automatic process, whereas identifying the color of the ink
 requires controlled processing. This conflict leads to slower
reaction times and increased errors in the incongruent condition,
demonstrating cognitive interference.
■ b. Go/No-Go Task
■ Purpose: Tests impulse control and response inhibition.
■ Design: Participants respond to a frequent "Go" stimulus but must
withhold their response when a rare "No-Go" stimulus appears.
■ Findings: Errors on "No-Go" trials indicate challenges in inhibiting
automatic responses.
■ c. N-Back Task
■ Purpose: Assesses working memory and updating.
■ Design: Participants must determine whether the current stimulus
matches the one presented n steps earlier.
■ Findings: Performance accuracy decreases as the value of n
increases, reflecting working memory demands.
○ d. Task-Switching Paradigm
■ Purpose: Evaluates cognitive flexibility.
■ Design: Participants switch between different tasks (e.g., categorizing
shapes by color in one trial and by size in the next).
■ Findings: Longer reaction times during task switches indicate the
cognitive effort required for flexibility.
○ 2. Neuroimaging Studies
These studies provide insights into the brain regions involved in cognitive control.
■ a. Functional Magnetic Resonance Imaging (fMRI)
■ Purpose: Measures brain activity by detecting changes in blood
flow.
■ Applications: Identifies areas like the prefrontal cortex (DLPFC,
ACC) active during tasks requiring cognitive control.
■ Example: Using fMRI during a Stroop Task to visualize conflict
monitoring in the ACC.
■ b. Electroencephalography (EEG)
■ Purpose: Records electrical activity of the brain.
■ Applications: Captures brain responses to specific events, such
as error detection and conflict (e.g., error-related negativity
(ERN)).
■ Example: Analyzing ERPs during a Go/No-Go task to study
real-time inhibition.
■ c. Positron Emission Tomography (PET)
■ Purpose: Measures metabolic activity or neurotransmitter levels.
■ Applications: Can identify changes in brain activity related to
sustained cognitive effort.
○ 3. Lesion Studies
■ Purpose: Examine the effects of damage to specific brain regions on
cognitive control.
 ■ Design: Studies individuals with brain injuries (e.g., damage to the
prefrontal cortex) to observe changes in decision-making, impulse
control, and flexibility.
■ Example: The famous Phineas Gage case demonstrated how prefrontal
cortex damage impairs emotional regulation and decision-making.
○ 4. Transcranial Magnetic Stimulation (TMS)
■ Purpose: Temporarily disrupts activity in targeted brain regions to study
their role in cognitive control.
■ Applications: Inhibiting the DLPFC can impair performance on tasks
requiring working memory or flexibility.
■ Example: Using TMS during a task-switching experiment to observe how
disruption of specific areas affects performance.
○ 5. Developmental and Longitudinal Studies
■ Purpose: Investigate how cognitive control develops over time or is
influenced by aging or experience.
■ Design: Researchers assess cognitive control at different ages or track
individuals over time.
■ Findings: Cognitive control improves during childhood and adolescence
(linked to prefrontal cortex maturation) and may decline with age.
○ 6. Computational Modeling
■ Purpose: Create models to simulate brain activity and cognitive
processes underlying control.
■ Applications: Helps predict how changes in neural connectivity or
neurotransmitter levels affect performance in cognitive tasks.
● Summary
Different experimental approaches offer complementary insights:
○ Behavioral tasks assess performance.
○ Neuroimaging reveals brain activity.
○ Lesion and stimulation studies show causal relationships.
○ Developmental and computational studies explore how cognitive control
changes over time or under different conditions.
● What does this test reveal about cognitive control? (second picture on Pebblepad)
● Which methods do we use in our cognitive control?
1. Goal Setting and Prioritization
○ What It Involves:
■ Setting clear objectives and deciding which tasks or goals are most
important.
■ Allocating mental resources accordingly.
○ Example: Creating a to-do list and focusing on the most urgent tasks first.
●
2. Attention Regulation
○ What It Involves:
■ Directing attention to relevant stimuli while ignoring distractions.
■ Sustaining focus on tasks, even when tempted to shift attention.
 ○ Example: Focusing on studying in a noisy environment by tuning out background
noise.
●
3. Inhibitory Control
○ What It Involves:
■ Suppressing automatic or impulsive responses that might interfere with
achieving a goal.
○ Example: Resisting the urge to check your phone while working on an important
assignment.
●
4. Working Memory Usage
○ What It Involves:
■ Holding and manipulating information in the mind for short periods to
complete tasks.
○ Example: Remembering a phone number long enough to dial it or keeping track
of instructions while cooking.
●
5. Cognitive Flexibility
○ What It Involves:
■ Switching between different tasks, strategies, or perspectives as needed.
○ Example: Switching from brainstorming creative ideas to editing a report with a
critical eye.
●
6. Error Monitoring and Self-Correction
○ What It Involves:
■ Recognizing mistakes or conflicts and adjusting behavior accordingly.
○ Example: Noticing you’ve misunderstood a task requirement and revising your
approach.
●
7. Emotional Regulation
○ What It Involves:
■ Managing emotional responses to maintain focus and decision-making.
○ Example: Staying calm and composed during a stressful meeting to
communicate effectively.
●
8. Task Planning and Execution
○ What It Involves:
■ Breaking down complex tasks into smaller, manageable steps.
■ Following through systematically.
○ Example: Planning how to study for multiple exams by allocating specific days
for each subject.
●
9. Mental Simulation and Anticipation
 ○ What It Involves:
■ Imagining future scenarios to predict outcomes and plan responses.
○ Example: Visualizing how a presentation will unfold and preparing answers for
potential questions.
●
10. Habit Formation and Automation
○ What It Involves:
■ Turning frequently performed tasks into habits to reduce cognitive load.
○ Example: Automatically preparing your workspace in the morning to minimize
decision fatigue.
●
Real-Life Applications:
○ Driving: Monitoring traffic (attention), following rules (inhibition), and adapting to
unexpected situations (flexibility).
○ Studying: Managing distractions, remembering key information, and adapting
study strategies.
○ Social Interactions: Adjusting your behavior depending on the social context or
managing conflicts.
● What happens if we lose control? Disorders that refer to losing cognitive control.
○ 1. Attention-Deficit/Hyperactivity Disorder (ADHD)
■ Key Issues:
■ Difficulty sustaining attention.
■ Impulsivity and hyperactivity.
■ Trouble with task organization and time management.
■ Connection to Cognitive Control:
■ Impaired inhibitory control (trouble suppressing distractions or
impulsive actions).
■ Weakened working memory and task flexibility.
■ Brain Areas Affected: Prefrontal cortex, particularly the dorsolateral
prefrontal cortex (DLPFC).
○ 2. Obsessive-Compulsive Disorder (OCD)
■ Key Issues:
■ Intrusive, repetitive thoughts (obsessions) and ritualistic behaviors
(compulsions).
■ Difficulty in stopping or switching off repetitive behaviors.
■ Connection to Cognitive Control:
■ Impaired inhibitory control prevents individuals from halting
compulsive actions.
■ Dysfunction in error monitoring leads to persistent feelings of
incompleteness.
■ Brain Areas Affected: Orbitofrontal cortex (OFC) and anterior cingulate
cortex (ACC).
○ 3. Schizophrenia
■ Key Issues:
 ■ Disorganized thinking, delusions, and hallucinations.
■ Difficulty distinguishing between relevant and irrelevant
information.
■ Connection to Cognitive Control:
■ Impaired working memory and flexibility.
■ Issues with error monitoring and adjusting behavior.
■ Brain Areas Affected: Prefrontal cortex and hippocampus.
○ 4. Major Depressive Disorder (MDD)
■ Key Issues:
■ Persistent low mood, negative thought patterns, and difficulty
concentrating.
■ Problems with decision-making and planning.
■ Connection to Cognitive Control:
■ Deficits in cognitive flexibility, leading to rigid negative thinking.
■ Weakened working memory, impairing goal-oriented tasks.
■ Brain Areas Affected: Dorsolateral prefrontal cortex (DLPFC), amygdala.
○ 5. Bipolar Disorder
■ Key Issues:
■ Alternating episodes of mania (elevated mood, impulsivity) and
depression.
■ Impaired judgment and risk-taking during manic episodes.
■ Connection to Cognitive Control:
■ Poor inhibitory control during mania leads to impulsive
behaviors.
■ Difficulty maintaining goal-directed behavior.
■ Brain Areas Affected: Prefrontal cortex, amygdala, and anterior
cingulate cortex.
○ 6. Substance Use Disorders
■ Key Issues:
■ Compulsive substance use despite negative consequences.
■ Difficulty resisting cravings.
■ Connection to Cognitive Control:
■ Impaired inhibitory control and decision-making.
■ Habitual behavior overrides rational decision-making.
■ Brain Areas Affected: Prefrontal cortex and basal ganglia.
○ 7. Frontotemporal Dementia (FTD)
■ Key Issues:
■ Personality changes, impulsivity, and difficulty with executive
tasks.
■ Loss of social inhibition and inappropriate behavior.
■ Connection to Cognitive Control:
■ Severe impairments in inhibitory control and emotional
regulation.
 ■ Brain Areas Affected: Frontal and temporal lobes, particularly the
prefrontal cortex.
○ 8. Parkinson’s Disease
■ Key Issues:
■ Motor symptoms (tremors, rigidity) alongside cognitive deficits.
■ Difficulty with task switching and problem-solving.
■ Connection to Cognitive Control:
■ Impaired flexibility and working memory.
■ Difficulty in initiating or halting movements or actions.
■ Brain Areas Affected: Basal ganglia and prefrontal cortex.
○ 9. Alzheimer’s Disease
■ Key Issues:
■ Memory loss, disorientation, and difficulty planning or organizing.
■ Connection to Cognitive Control:
■ Impaired working memory and goal-directed behavior.
■ Decline in flexibility and inhibitory control.
■ Brain Areas Affected: Prefrontal cortex and hippocampus.
○ 10. Impulse Control Disorders (e.g., Intermittent Explosive Disorder,
Kleptomania)
■ Key Issues:
■ Sudden episodes of impulsive, aggressive, or destructive
behavior.
■ Difficulty resisting urges to perform harmful actions.
■ Connection to Cognitive Control:
■ Severe deficits in inhibitory control.
■ Brain Areas Affected: Ventromedial prefrontal cortex (vmPFC),
amygdala.
● Implications of Losing Cognitive Control
When cognitive control is compromised, individuals struggle to adapt their behaviors to
the demands of the environment. This can result in:
○ Poor decision-making.
○ Difficulty regulating emotions.
○ Inability to inhibit harmful or maladaptive behaviors.

Brain Motor Control

● Motor Control?
Motor control refers to the ability of the nervous system to regulate and direct the
body's movements. It involves the coordination of muscles, joints, and sensory inputs to
produce smooth, accurate, and purposeful motion. Here's a breakdown of its key
components:
○ 1. Levels of Motor Control
 ■ Reflexive Control: Automatic, involuntary responses (e.g., knee-jerk
reflex).
■ Voluntary Control: Conscious and intentional movements (e.g., reaching
for an object).
■ Automatic Control: Semi-conscious actions (e.g., walking, typing).
○ 2. Neuroanatomy Involved
■ Motor Cortex: Initiates voluntary movements.
■ Basal Ganglia: Modulates movement, ensuring smooth execution.
■ Cerebellum: Fine-tunes movements and maintains balance.
■ Spinal Cord: Pathway for transmitting motor commands from the brain to
the muscles.
■ Sensory Feedback Systems: Provide real-time updates to adjust
movements.
○ 3. Types of Movements
■ Gross Motor Skills: Involve large muscle groups (e.g., running, jumping).
■ Fine Motor Skills: Involve precise movements using smaller muscles
(e.g., writing, buttoning a shirt).
○ 4. Motor Learning
■ The process by which we acquire or modify motor skills through practice
and experience. It involves stages:
1. Cognitive Stage: Understanding what needs to be done.
2. Associative Stage: Refining the movement pattern.
3. Autonomous Stage: Performing the skill effortlessly.
○ 5. Disorders of Motor Control
■ Parkinson’s Disease: Affects basal ganglia, leading to tremors, rigidity.
■ Cerebellar Ataxia: Impaired coordination due to cerebellum damage.
■ Cerebral Palsy: A group of disorders affecting movement and posture.
● How do different brain regions and pathways integrate to create complex motor
behaviors?
Complex motor behaviors, such as walking, playing a musical instrument, or writing,
require the coordinated activity of multiple brain regions and neural pathways. These
behaviors rely on the integration of sensory input, motor planning, execution, and
feedback correction. Below is an outline of how different brain regions and pathways
contribute:
○ Key Brain Regions Involved in Motor Control:
■ Primary Motor Cortex (M1):
1. Located in the precentral gyrus, it directly controls voluntary
muscle movements.
2. Neurons in M1 send signals via the corticospinal tract to motor
neurons in the spinal cord, which innervate muscles.
■ Premotor Cortex:
1. Involved in planning and coordinating complex movements.
2. Integrates sensory information and helps in the selection of
appropriate movements in response to external stimuli.
 ■ Supplementary Motor Area (SMA):
1. Responsible for internally generated movements, such as those
based on memory or intent.
2. Plays a key role in coordinating bilateral movements (e.g.,
clapping).
■ Basal Ganglia:
1. A group of subcortical nuclei (including the caudate, putamen, and
globus pallidus) that regulate movement initiation, motor learning,
and habit formation.
2. Modulate motor commands from the cortex and ensure smooth
execution by suppressing unwanted movements.
■ Cerebellum:
1. Critical for motor coordination, precision, and timing.
2. Receives sensory input and motor commands, compares them,
and adjusts movements to maintain balance and accuracy.
■ Thalamus:
1. Acts as a relay station, transmitting motor signals between the
cortex, basal ganglia, and cerebellum.
2. Also integrates sensory feedback necessary for motor control.
■ Brainstem:
1. Contains motor nuclei involved in basic movements (e.g., posture,
locomotion) and reflexes.
2. Includes pathways like the vestibulospinal tract for balance and
reticulospinal tract for locomotion.
○ Motor Pathways:
■ Corticospinal Tract:
1. The primary pathway for voluntary motor control.
2. Signals travel from the motor cortex, through the brainstem, and to
the spinal cord to innervate skeletal muscles.
■ Corticobulbar Tract:
1. Similar to the corticospinal tract but controls facial and cranial
muscles.
■ Extrapyramidal System:
1. Includes pathways such as the rubrospinal, reticulospinal, and
vestibulospinal tracts.
2. Regulates subconscious motor activity, such as posture and
balance.
● What happens when specific components of this motor system are damaged?
Damage to different components of the motor system leads to distinct motor deficits,
depending on the location and extent of the injury:
○ Primary Motor Cortex:
■ Lesions result in weakness or paralysis of voluntary movements on the
opposite side of the body (hemiparesis or hemiplegia).
■ Fine motor skills, like writing, are often more affected.
 ○ Premotor and Supplementary Motor Areas:
■ Damage leads to difficulties in motor planning (apraxia) despite intact
muscle strength.
■ For example, patients may struggle to perform learned movements on
command.
○ Basal Ganglia:
■ Disorders include Parkinson's disease (hypokinetic) and Huntington's
disease (hyperkinetic).
■ Symptoms can range from tremors, rigidity, and bradykinesia (slowness)
to involuntary, excessive movements (chorea).
○ Cerebellum:
■ Lesions cause ataxia, characterized by uncoordinated, clumsy
movements.
■ Patients may experience tremors during purposeful movement,
imbalance, and difficulty with precise motor tasks.
○ Spinal Cord or Corticospinal Tract:
■ Leads to spasticity (increased muscle tone), weakness, or paralysis
depending on the level of damage.
■ Reflexes may be exaggerated (hyperreflexia).
○ Brainstem:
■ Damage can affect both motor and autonomic functions, potentially
leading to severe issues like locked-in syndrome, where voluntary
movement is largely impossible except for eye movements.
● What is readiness potential?
Readiness potential (RP), or Bereitschaftspotential, is a specific type of brain activity
detected using electroencephalography (EEG) that occurs before voluntary motor
actions.
○ Key Features:
■ RP reflects the brain's preparation for movement and arises about 1-2
seconds before a voluntary action.
■ It originates primarily from the SMA and premotor cortex, with later
contributions from the primary motor cortex.
■ RP consists of two phases:
1. Early RP: A gradual buildup of activity, originating from the SMA.
2. Late RP: A sharper increase in motor cortex activity just before
the movement.
○ Significance:
■ Readiness potential suggests that motor preparation begins
unconsciously before the individual becomes aware of their intention to
act.
■ Studies on RP have contributed to debates in neuroscience and
philosophy regarding free will, as the brain appears to "decide" on an
action before conscious intent is recognized.
 ● Different things that can affect the motor control?
Motor control is sensitive to a wide range of factors, including:
Neurological Conditions:
○ Stroke, Parkinson's disease, multiple sclerosis, or cerebral palsy can impair
motor pathways.
● Sensory Impairments:
○ Loss of proprioceptive input (body awareness) or vision can disrupt fine motor
control and balance.
● Psychological Factors:
○ Stress and anxiety can impair motor performance, leading to tremors or muscle
stiffness.
● Fatigue:
○ Physical or mental exhaustion can reduce motor efficiency and increase error
rates.
● Age:
○ Motor control naturally declines with age, often due to degeneration in the basal
ganglia, cerebellum, and motor cortex.
○ How alcohol and drugs can influence motor functions?
Alcohol:
■ Alcohol depresses the central nervous system (CNS), impairing
coordination, balance, and reaction times.
■ It disrupts cerebellar function, causing symptoms like ataxia and slurred
speech.
■ Chronic alcohol use can lead to peripheral neuropathy, further impairing
motor control.
○ Drugs:
■ Stimulants (e.g., cocaine, amphetamines) can cause hyperactivity and
tremors by overstimulating motor pathways.
■ Opioids and benzodiazepines suppress motor activity, leading to slowed
reflexes and poor coordination.
■ Cannabis affects motor timing and spatial awareness, primarily by
modulating cerebellar and basal ganglia activity.

Lateralization
● 1. What is Lateralization? (Expanded)
Lateralization refers to the specialization of brain functions in the left and right
hemispheres of the cerebral cortex. While both hemispheres are capable of handling
most cognitive functions, certain processes are more dominant in one hemisphere than
the other. This specialization is essential for efficient brain processing, as it allows for
parallel processing—the ability of the brain to handle multiple tasks at once.
 Key Features of Lateralization
1. Hemispheric Specialization
Each hemisphere has specific cognitive strengths and processes.
○ Left Hemisphere (Logical/Analytical)
■ Language and Speech: This hemisphere is dominant for most people in
language production (via Broca’s area) and language comprehension (via
Wernicke’s area).
■ Analytical and Logical Thinking: The left hemisphere processes
information step-by-step, making it essential for tasks like
problem-solving, logic, and critical thinking.
■ Mathematics and Calculations: Analytical tasks, such as math and
numerical reasoning, are managed by the left hemisphere.
■ Detail-Oriented Processing: The left hemisphere focuses on specifics,
like analyzing smaller details to create a bigger picture.
○ Right Hemisphere (Creative/Spatial)
■ Spatial Awareness and Visual-Spatial Processing: The right
hemisphere helps you recognize faces, navigate space, and process
maps or spatial relationships.
■ Creativity and Artistic Ability: This hemisphere is more active during
creative thinking, imagination, and artistic pursuits like drawing, music,
and dance.
■ Emotion Recognition: The right hemisphere plays a larger role in
understanding nonverbal communication, such as facial expressions,
gestures, and emotional intonation in voices.
■ Holistic/Big-Picture Processing: While the left hemisphere processes
parts of information, the right hemisphere processes whole patterns,
helping to see "the bigger picture."
■ Music Perception: While rhythm processing may involve the left
hemisphere, melody and emotional aspects of music are often processed
in the right hemisphere.
●
2. Handedness and Language Lateralization
○ Right-Handed People: For about 90-95% of right-handed people, language
processing is dominant in the left hemisphere.
○ Left-Handed People: Language lateralization is more variable in left-handed
individuals, with about 70% still showing left-hemisphere dominance, while 15%
have right-hemisphere dominance, and 15% have shared dominance (bilateral
processing).
○ Ambidextrous People: Their language lateralization is similar to left-handers,
but it tends to be more bilateral.
●
3. Sex Differences in Lateralization
 ○ Male Brains: Some studies suggest that males have a stronger lateralization of
language and spatial processing, meaning functions are more strictly separated
between hemispheres.
○ Female Brains: Female brains often show more bilateral activation during tasks,
meaning they engage both hemispheres for processes like language and spatial
reasoning. This may contribute to differences in multitasking abilities and
emotional processing.
●
4. The Role of the Corpus Callosum
The corpus callosum is a thick bundle of nerve fibers that connects the left and right
hemispheres, enabling communication between them. It allows both hemispheres to
coordinate activities and share information. In people with a severed or underdeveloped
corpus callosum (like those with agenesis of the corpus callosum or after a split-brain
procedure), the hemispheres work more independently, revealing the specific functions
of each hemisphere.

Why Lateralization Matters

○ Efficiency: Lateralization allows for more efficient brain processing. For
example, while the left hemisphere focuses on language and fine motor control,
the right hemisphere can simultaneously process spatial and emotional
information.
○ Dual Processing: By dividing tasks between hemispheres, the brain can
process multiple types of information at once.
○ Evolutionary Benefit: Lateralization is seen in other species too (like birds and
primates), suggesting it is an evolutionary adaptation that supports survival by
enabling complex motor, social, and cognitive behaviors.
● 2. Split-Brain Procedure
A split-brain procedure, or corpus callosotomy, is a surgery that severs the corpus
callosum (the band of neural fibers connecting the hemispheres). This procedure is
typically done to control severe epilepsy when seizures spread between hemispheres.
The Italian Study (Gazzaniga & Sperry)
○ Participants: Patients who had undergone a corpus callosotomy.
○ Method: Researchers presented visual information to one hemisphere at a time
(via the visual field) and studied patients' ability to process and respond to it.
○ Findings:
■ Left Hemisphere (Language-Dominant): Patients could describe
objects seen in the right visual field(processed by the left hemisphere).
■ Right Hemisphere (Non-Verbal Perception): When an object was
presented in the left visual field(processed by the right hemisphere),
patients could not verbally identify it but could draw or pick it out with their
left hand.
■ Significance: This demonstrated that the two hemispheres process
information independently when the corpus callosum is severed.
● 3. Differences in Stroke Damage Between Left and Right Hemispheres
A stroke occurs when blood flow to part of the brain is blocked, leading to cell death. The
side of the brain affected influences the type of impairment experienced.
Left Hemisphere Stroke Damage
○ Aphasia (Language Deficits): Difficulty speaking, understanding language,
reading, or writing.
■ Broca’s Aphasia: Struggle to produce speech but comprehension is
intact.
■ Wernicke’s Aphasia: Fluent but nonsensical speech with poor
comprehension.
○ Right-Sided Paralysis: The left hemisphere controls motor functions on the right
side of the body.
○ Analytical/Logical Deficits: Problems with tasks requiring logic, math, and
analytical reasoning.
○ Mood Changes: Increased likelihood of experiencing depression and anxiety.
● Right Hemisphere Stroke Damage
○ Left-Sided Paralysis: The right hemisphere controls motor functions on the left
side of the body.
○ Spatial Neglect: Failure to recognize or attend to the left side of objects or space
(left-side neglect).
○ Emotion/Facial Recognition Deficits: Difficulty processing emotional
expressions and social cues.
○ Artistic and Creative Deficits: Impairments in music, art, and visual-spatial
skills.
○ Impulsive Behavior: Poor awareness of deficits, leading to risky behavior.
● 4. Models of Left Hemisphere Language Systems
Several models explain how the left hemisphere supports language processing. Here are
the main models:
1. Wernicke-Geschwind Model
○ Core Idea: Language processing relies on specific brain regions, and
communication occurs between them.
○ Key Structures:
■ Broca’s Area: Responsible for speech production.
■ Wernicke’s Area: Responsible for language comprehension.
■ Arcuate Fasciculus: A fiber bundle connecting Wernicke’s and Broca’s
areas.
○ Pathway:
■ Heard words → Auditory Cortex → Wernicke’s Area (comprehension) →
Arcuate Fasciculus → Broca’s Area (speech production) → Motor Cortex
(to move mouth, tongue, etc.).
○ Limitations: Overly simplistic; other areas also play a role in language.
● 2. Dual-Stream Model (Hickok & Poeppel)
○ Core Idea: There are two streams of language processing.
 ■ Dorsal Stream (Where/How): Maps speech sounds to motor
representations for speech production.
■ Ventral Stream (What): Maps speech sounds to their meanings
(semantic processing).
○ Key Difference: This model emphasizes parallel processing rather than a single
pathway.
● 3. Connectionist Models
○ Core Idea: Neural networks and connections, rather than isolated areas, support
language processing.
○ How it Works: Language processing occurs through distributed processing
across several brain areas, and the connections between them are crucial.
○ Why It Matters: This model reflects a more modern, accurate understanding of
how the brain processes language, accounting for both the left and right
hemispheres.

Stroke Overview
Definition of Stroke

● A stroke is a medical emergency characterized by a sudden disruption of blood flow to

the brain, leading to brain cell damage due to oxygen deprivation .

Types of Stroke

1. Ischemic Stroke:
○ Accounts for about 85% of strokes; occurs when a blood clot obstructs blood flow
to the brain .
○ Causes:
■ Thrombotic Stroke: Blood clot forms in an artery in the brain due to fatty
deposits .
■ Embolic Stroke: A clot forms elsewhere (often the heart) and travels to the
brain .
2. Hemorrhagic Stroke:
○ Less common but often more severe; occurs when a blood vessel ruptures,
causing bleeding in the brain .
○ Types:
■ Intracerebral Hemorrhage: Bleeding occurs directly in the brain .
■ Subarachnoid Hemorrhage: Bleeding occurs in the space between the
brain and surrounding tissue .
3. Transient Ischemic Attack (TIA):
○ Often called a mini-stroke; temporary blockage of blood flow that resolves within
minutes to hours without permanent damage .
Recognizing Stroke Symptoms

● The BFAST acronym helps identify stroke symptoms:

○ Balance: Sudden loss of balance.
○ Face: One side of the face droops.
○ Arms: Inability to raise one arm.
○ Speech: Slurred speech or difficulty speaking.
○ Time: Call emergency services immediately if any symptoms are present .

Treatment Options

● Ischemic Stroke:
○ Thrombolytic Drugs: Dissolve blood clots; most effective within 3-4 hours of onset
.
○ Mechanical Thrombectomy: Physical removal of the clot .
● Hemorrhagic Stroke:
○ Focus on controlling bleeding and reducing pressure on the brain, often requiring
surgical interventions like clipping or coiling .

Risk Factors

● Non-modifiable: Age, family history, previous strokes .

● Modifiable: High blood pressure, heart disease, diabetes, smoking, obesity, excessive
alcohol consumption, and chronic stress .

Brain Regions Affected by Stroke

● Cerebral Cortex: Higher cognitive functions; damage can lead to various symptoms .
● Motor Cortex: Controls voluntary movements; damage can cause paralysis on the
opposite side of the body .
● Broca's Area: Speech production; damage leads to Broca's aphasia .
● Wernicke's Area: Language comprehension; damage leads to Wernicke's aphasia .
● Basal Ganglia: Involved in movement control; damage can lead to movement disorders .
● Cerebellum: Coordination and balance; damage can cause ataxia .
● Brain Stem: Vital functions like breathing and heartbeat; damage can be life-threatening .

Cognitive and Motor Impairments

● Cognitive Control: Impairments can affect planning, problem-solving, and emotional

regulation .
● Motor Functioning: Includes hemiparesis (partial weakness), hemiplegia (complete
paralysis), spasticity, and apraxia (difficulty with motor planning) .

Rehabilitation and Recovery

● Neuroplasticity: The brain's ability to reorganize itself; critical for recovery .

 ● Rehabilitation Goals: Focus on improving physical, cognitive, communication, and mood
functions .
● Therapies:
○ Physical Therapy: Aims to regain motor function and mobility .
○ Speech Therapy: Focuses on rebuilding communication skills .
○ Cognitive Rehabilitation: Targets cognitive control and executive functions .

Conclusion

● Stroke can have profound effects on individuals, impacting their physical, cognitive, and
emotional well-being. Early recognition and treatment are crucial for improving outcomes
and recovery.

Vision
● Rods = scotopic vision, no color, vision in dim lighting
● Cones = photopic vision, color, vision in bright lighting
● Bipolar cells
○ Bipolar cells receive information from photoreceptors and pass that information
on to the ganglion cells
● Retinal ganglion cells
○ Conduct action potentials with information from the bipolar cells and send it to the
brain via the optic nerve (which is mostly comprised of ganglion cells’ axons)
● Horizontal cells: modulate signals between photoreceptors and bipolar cells.
○ They contribute to adaptation to light and contrast.
● Amacrine cells: connected with the bipolar and ganglion cells
○ They modulate the signals between bipolar cells and ganglion cells
○ They detect motion
● Rods, cones, bipolar cells and horizontal cells only generate graded local potentials, do
not produce action potentials, and they affect each other by the release of
neurotransmitters (Glutamate = excitatory, GABA = inhibitory, etc.)
● Photopigments (rhodopsin and photopsin)
● Types and functions of cells in the retina

● Phototransduction in rods and cones converts light into electrical signals

● Phototransduction or photoisomerization
● A photopigment (chemical molecule) interacts with light, undergoing a structural change.
Light interacts with rhodopsin, changing the shape of retinol. This causes Na+/Ca2+ ion
channels to close, thereby causing the hyperpolarization of the photoreceptor cell. This
leads to the release of glutamate.
● In the dark, there is no conformational change in rhodopsin, which means that the
Na+/Ca2+ ion channels remain open, which means that the photoreceptor cell is
depolarized, which means that glutamate is released.
● In the light, there is conformational change in rhodopsin, which means that the
Na+/Ca2+ ion channels close, which means that the photoreceptor cell is
hyperpolarized, which means that glutamate is not released.
● On center and off center bipolar cells
● When glutamate binds to On center bipolar cells, they become depolarized
● When glutamate binds to Off center bipolar cells, they become hyperpolarized
● Depolarized bipolar cells increase neurotransmitter (glutamate)release
● Hyperpolarized bipolar cells decrease neurotransmitter (glutamate) release
● The glutamate binds to receptors on the membrane of ganglion cells
● The binding of glutamate causes the generation of an action potential in the ganglion cell
● This action potential travels to the brain, and specifically to the visual cortex (occipital
lobe)
 ● Dark surround, light middle, off bipolar cell, inhibiting the release of glutamate, ganglion
cells fire slowly, image b) in pebblepad
●

MC QUESTIONS

What are the two main types of photoreceptors?

a)Cones and Ganglions
b) Rods and Cones
c)Ganglions and Rods

Which of the following is correct?

a. Photoreceptors are normally in a hyperpolarized state, meaning that their inner membrane
potential is less negative than the surrounding extracellular fluid. (Depolarised state)
b. Bipolar cells depolarize, meaning their membrane potential becomes more positive, so that
they are now able to transmit the signal onward to ganglion cells.
c. Depolarisation occurs when the influx of sodium ions is reduced and potassium ions (K⁺)
leave the cell. (Hyperpolarization)
what are the pigments in cones called?

a) codopsin
b) iodopsin
c) rhodopsin

What happens when glutamate binds to an On center bipolar cell?

a. the cell depolarizes, therefore increasing its glutamate release.

b. the cell hyperpolarizes, therefore increasing its glutamate release.

c. the cell hyperpolarizes, therefore decreasing its glutamate release.

Which type of photoreceptor is responsible for color vision?

A) Rods
B) Cones
C) Bipolar cells
Correct Answer: B) Cones

Consider an OFF bipolar cell that synapses with three photoreceptors (two surround and one
center), and with one retinal ganglion cell (RGC). What happens to the release of glutamate in
the synapse between the bipolar cell and the RGC if you have an image with a dark center and
a light surround?
A. High release of glutamate
B. Low release of glutamate
C. No release of glutamate

Which statement is correct?

A: The horizontal cells contact the photoreceptors and the bipolar cells
B: the horizontal cells contact the bipolar cells and the ganglion cells
C: The horizontal cells contact the photoreceptors and the ganglion cells.

VIDEOS to help understand → added by tutor

Online Materials The Eye and the Retina:
https://www.youtube.com/watch?v=fZDAwXh54is (2min Neuroscience - The Retina)
https://www.youtube.com/watch?v=dhd2fja0LZ4 (2min Neuroscience - Phototransduction)
https://www.youtube.com/watch?v=hsh2kPdgazo (National geographic Eye)
http://www.youtube.com/watch?v=Z8asc2SfFHM
http://www.youtube.com/watch?v=ajnsDVsP0Uk
http://www.youtube.com/watch?v=AuLR0kzfwBU&feature=related (molecular mechanisms of
phototransduction)
Center-surround antagonism:
https://www.youtube.com/watch?v=NkumQb-zMQM
https://www.youtube.com/watch?v=1D_nIIevdzc
https://www.youtube.com/watch?v=jTEqoefv-pY
https://www.youtube.com/watch?v=0gYS5dtdbc4
https://www.youtube.com/watch?v=4jJS4MnkcWw
https://www.sumanasinc.com/webcontent/animations/content/receptivefields.html
Hermann Grid -

1. What areas are most involved in the processing of vision and the process of the action
potential: Visual pathway from the retina to the brain regions
Retina
- Collects information
Optic nerve
- Sends information to the brain
Optic chiasm
- Point where two optic nerves cross
LGN(Lateral geniculate Nucleus)
- Located in the Thalamus
- Area organises information and sends it to the visual cortex
- 6 main layers
- Parvocellular 4 external layers. Involved in color discrimination
- Magnocellular: 2 internal layers. Not involved in color discrimination(cannot differentiate
wave lengths)

Primary Visual Cortex(V1)

- Analyses information
- The information is then sent to the visual association areas
Visual association areas
 - Brain recognises shapes, patterns and objects

2. Research the primary visual cortex and understand the diagram. (color coded one)
● Located in the occipital lobe
● V1/brodmann's area 17/ Striate Cortex/ visual receiving area
● 4 main dimensions of the visual stimulus:
- location of the visual field,
- ocular dominance (specified columns, all cells in a vertical column have the same
ocular dominance),
- orientation
- color.

Retinal topic organization: V1 is a topographic field of the organization of cells

Location column: all the neurons within a location column have their receptive fields at the same
location on the retina.

- Hypercolumn: black boxes in the diagram

- Co Blobs: assembled in a cylindrical shape and they lie above and below the layer 4
- Input from the retina goes to cortical layer 4. (magnocellular: 4c, 4a, parvocellular 4c, 4a,
4b)
3. What are the most important processing stages of the visual system,
4. What are the different pathways that appear?
- M pathway: responsible for perceiving objects and for guiding the way towards
them.
- P pathway: visually identifying objects
- Single cortical cells(orientation columns) respond to edge or bars with particular
width/orientation in the visual field, sometimes called bar detectors or edge
detectors
- Complex cortical cells responsible for movement
- N stop Cells: verify corners and edges and object permanence
- Orientation density curve(for single neurons): normal curve and in the centre
highest firing frequency at 90 degree orientation.

5. What are the types of visual information?

 ● Dorsal Pathway: motion is handled Passes through layer 4 of V1 to V2 to V3 then
it skips V4 and goes to V5(middle temporal visual area) then splits into Ventral
Intraparietal and Medial superior lobe
● Ventral Pathway: Object and face recognition, form and shape recognition.
Passes through layer 4 of V1(primary visual cortex) to V2 (prestriate cortex or
secondary visual cortex) skips V3 and goes directly to V4 (visual area 4 part of
the extrastriate visual cortex) and ends at the inferior temporal lobe.

6. Differences between large and small ganglion cells?

- M(large ganglion cells): larger receptive fields involved in processing information
about motion and changes in visual stimuli. (responsible for where?)
- P(small ganglion cells):smaller receptive fields involved in processing information
about fine details(colour and brightness) (responsible for what?)

7. Link the cases mentioned in 3B to the concept of single/double dissociation.

- Single Dissociation: if you have one area with a lesion you conclude that the lesion area
is affecting and has certain behaviour.
- Double Dissociation: comparing two cases with lesions to be more sure that the lesions
affect certain abilities.
- DF lost the ability to perceive faces and objects but could reach for them caused by
damage to the ventral stream
- RV: could identify but could not reach for them caused by damaged dorsal stream

8. What do the grasp lines show to try to explain the last diagram?

9. Create own MC question

○ 1. Primary visual system: Some axons continue to the thalamus and terminate
in the lateral geniculate nucleus (LGN). They then form the optic radiations
which project to the primary visual cortex (V1, located on the medial surface).
○ 2. Pupillary light reflex pathway: While, some others go to the midbrain (in the
pretectum) where they are responsible for pupillary light reflex and accommodation
reflex.
○ 3. Tectospinal pathway: Other fibers fo to the superior colliculus a region in
the brain stem that help coordinate eye and head movement
○ 4. Retinohypothalamic pathway: Other fibers go to a region of the
hypothalamus, the suprachiasmatic nucleus. Which helps maintain circadian or
daily rhythms

MC QUESTIONS
Which structure is responsible for transmitting action potentials that are generated from
the left lateral visual field to the neurons of the optic chiasm?
A) Temporal fibers
B) Optic tract
C) Nasal fibers

Which visual pathway is primarily responsible for processing motion and orientation?
A) Parvocellular pathway
B) Magnocellular pathway
C) Koniocellular pathway
Correct Answer: B) Magnocellular pathway

Which sentence is correct?

A) the ventral system is responsible for visually identifying objects
B) the dorsal system is responsible for visually identifying objects
the ventral system is responsible for perceiving the location of objects and guiding movements
toward them

Neuromodulation
- What is neuromodulation?
- Refers to the process by which certain substances in the brain regulate/modulate
its activity
- What are the main neuromodulators?
- Neurotransmitters: serotonin, dopamine, norepinephrine, oxytocin
- Dopamine: involved in reward, motivation, pleasure, motor control
- Associated disorders: parkinsons, loss of dopamine production,
schizophrenia, addiction
- Serotonin: regulates mood, emotion, sleep, appetite, digestion
- Associated disorders: depression, anxiety, OCD
- Norepinephrine: attention, arousal, fight or flight response
- Associated disorders: ADHD, depression, anxiety
- External stimulation: transcranial magnetic stimulation
- Use TMS to create lesions in the brain and thereby modulate its activity of
neurons.
- How is serotonin (5HT) dependent on/influenced by the food-derived precursor
tryptophan?
- Involved in the synthesis of serotonin in a two-step reaction
- Is an essential amino acid, meaning that the body does not produce it, therefore
it can only be ingested.
1. Dietary tryptophan is converted to
5-hydroxy-L-tryptophan (5-HTP) via an oxidation reaction by the enzyme tryptophan
hydroxylase
2. 5-HTP is then converted into 5-HT (serotonin) via a decarboxylation reaction by enzyme
aromatic L-amino acid decarboxylase (AADC)

- There can be one more step after production of serotonin -

- can then be converted to melatonin (circadian rhythm)
- Serotonin is synthesised in the brain, therefore tryptophan has to cross the blood
brain barrier
- There is more tryptophan (TRP) in the plasma compared to other amino
acids (LNAA), then it is more likely to diffuse through the blood brain
barrier.
- Figure in pebblepad:
- Plasma ratio TRP/LNAA determines amount of tryptophan across the
blood-brain barrier (BBB)
- Key mechanism: high TRP to LNAA ratio allows more tryptophan to
cross the BBB => increasing brain tryptophan level leads to higher
serotonin production
- Protein intake: increases level of TRP and LNAA but more significantly for LNAA
=> decrease of TRP/LNAA ratio which reduces brain serotonin synthesis
- Carbohydrates intake: carbohydrates stimulate insulin release; insulin reduces
LNAA level by promoting its reuptake into tissue (muscles) => TRP/LNAA ratio
increases which enhances tryptophan transport to brain and boosting serotonin
production
- Acute tryptophan depletion: consequence of self-consuming tryptophan -
decreases the ratio of tryptophan compared to other amino acids - reduction of
serotonin synthesis - has effects on mood
- People that are affected by this usually have a history of mood disorders,
genetic vulnerabilities, and seasonal mood disorder
- People with ‘healthy brains’ are not as affected by this
- What foods are beneficial for depression/anxiety and which cause more harm?
- Foods which contain tryptophan: Turkey, chicken, nuts, eggs, fish, soybeans,
bananas, cheese, yogurt, dairy products
 - Carbohydrates increase availability of tryptophan in the brain - helps with the
production of insulin which removes amino acids in the bloodstream, increasing
the ratio : rice, quinoa,
- Vegetarian options which contain tryptophan: soya, cashew nuts, dark chocolate
- Fatty acids reduce inflammation and support brain function - potentially reduce
levels of depression and anxiety
- Walnuts, flax seeds, chia seeds, fatty fish
- magnesium rich foods: leafy greens, spinach, almonds, avocado, dark chocolate
- Harmful foods: foods that are high in other amino acids other than tryptophan
- Alcohol, high processed fast foods, refined carbohydrates, sugary foods,
caffeine (emotional arousal, affect sleep)
- Refined carbohydrates can lead to more fatigueness and negative
moods
- How do proteins act as neuromodulators?
- Protein intake: increases level of TRP and LNAA but more significantly for LNAA
=> decrease of TRP/LNAA ratio which reduces brain serotonin synthesis
- Guy from pebblepad ate a lot of protein and not a lot of carbohydrates,
and this in turn caused a decrease in mood because it affected the ratio
of tryptophan to amino acids - does not mean that they are
neuromodulators.
- What are other ways/interventions (other than food) that can alter the brain?
- MDMA
- Hugging
- Alcohol
- Meditation
Antidepressants (selective serotonin reuptake inhibitors - SSRI’s)

Genetic Brain and Depression

Key Concepts

● Stress: Defined as the energy required to maintain balance in life amidst daily
challenges. Stress can be functional (adaptive) or dysfunctional (leading to health
issues) .
● Stress Hormones: In response to stress, hormones such as catecholamines, cortisol,
and adrenaline are produced. These hormones are essential for the body's adaptation to
stress .

Biological Mechanisms

● Dual Route of Stress Response: The brain responds to stress through two pathways:
 1. Quick and Dirty Route: Involves immediate responses from the amygdala and
hypothalamus, activating the HPA (Hypothalamus-Pituitary-Adrenal) axis .
2. Long-Term Route: Engages the prefrontal cortex for cognitive processing and
regulation of the initial response .
● Neurotransmitters: Key neurotransmitters involved in stress and depression include
serotonin, which is crucial for mood regulation. The serotonergic system's functionality is
linked to stress resilience .

Theories of Depression

● Diathesis-Stress Model: This model posits that individuals have a genetic predisposition
(diathesis) that interacts with environmental stressors, increasing vulnerability to
depression .
● Serotonin Hypothesis: Initially thought that depression arises from a shortage of
serotonin, but current understanding emphasizes the role of serotonergic receptors and
their regulation .

Genetic Factors

● Serotonin Transporter Gene: Variations in the serotonin transporter gene (5-HTTLPR)

influence the number of serotonin transporters in the brain. Individuals with the short
allele are more susceptible to stress-related disorders .
● Research Findings: Studies have shown that individuals carrying the short allele exhibit
greater stress responses and are at higher risk for developing depression following
stressful life events .

Coping Mechanisms

● Coping Styles: The ability to cope with stress varies among individuals. Those with
effective coping strategies are less likely to develop stress-related disorders .
● Personality Traits: Certain personality traits, such as high neuroticism, are associated
with increased vulnerability to stress and negative cognitive patterns .

Experimental Studies

● Acute Stress Tests: Various methods, such as cold exposure and social stress
scenarios, are used to study stress responses in participants. These studies help
elucidate the relationship between genetic predisposition and stress reactivity .

This summary encapsulates the key concepts and findings related to the genetic and
biochemical underpinnings of stress and depression, emphasizing the interplay between
biological predispositions and environmental factors.

Key Concepts in Nutritional Neuroscience and Mental Health

Gene-Environment Interactions
 ● The interaction between serotonergic genes and stress exposure has been studied
extensively, revealing that the effects on depression are not as strong as initially
believed. Inconsistencies in findings may arise from methodological differences and
citation bias, where studies showing effects are more likely to be published than those
that do not , .
● Psychological factors, such as cognitive vulnerability and stress attribution, play a
significant role in how individuals respond to stress and may influence the risk of
depression , .

Food and the Serotonergic System

● The relationship between food and the serotonergic system is a key area of interest.
Certain foods may influence serotonin levels in the brain, which is crucial for mood
regulation , .
● Tryptophan, an essential amino acid found in food, is necessary for serotonin synthesis.
It must be obtained from the diet, as the body cannot produce it , .
● Carbohydrates can increase serotonin levels by enhancing the uptake of tryptophan into
the brain. This occurs through an insulin response that directs other amino acids to the
muscles, allowing tryptophan to have a higher ratio in the bloodstream , .

Research Findings on Food and Mood

● Studies indicate that while carbohydrates may have limited beneficial effects on mood in
healthy populations, they can be more effective in individuals with certain vulnerabilities,
such as high neuroticism or chronic stress , .
● Research has shown that tryptophan-rich foods can reduce stress and depressive
symptoms, particularly in genetically vulnerable populations , .

Scientific Methodology and Claims

● The validity of claims regarding food and behavior must be assessed through rigorous
scientific methods, including randomized controlled trials and meta-analyses. It is crucial
to rely on a body of evidence rather than individual studies to draw conclusions , .
● Misinterpretations of research can lead to exaggerated claims about the addictive nature
of certain foods, which do not align with the scientific understanding of addiction and
reward systems , .

Conclusion

● The interplay between diet, genetics, and mental health is complex, with ongoing
research needed to clarify these relationships and their implications for treatment and
prevention strategies in mental health.
Podcast
https://notebooklm.google.com/notebook/8ea2f1c5-1167-459a-b10d-c03599aee76c/audio