Chapter 7 Study Guide

Zygote: egg fertilized by sperm, single cell

Blastula: hollow ball of cell when zygote starts dividing
Gastrula: 3 layered form of partially differentiated blastocyst
Embryo: Within a week, 3 layers, ectoderm, mesoderm, endoderm
- Ectoderm will form the NS
Fetus: recognizable in relation to mature form at around 10 weeks (can see head and
general form of limbs)
Gastrulation: hollow sphere of cells (blastula) invaginates and forms three layers of cell -
forms the gastrula
Neurulation: start of the development of the NS. The ectoderm (dorsal epithelial layer)
thickens to form the neural plate. The neural plate will fold to form the neural groove and
eventually the CNS
Development of the nervous system:
1. At around 18 days, the neural plate forms from the ectoderm.
2. At 20 days, the neural plate folds to form the neural groove and neural crest
3. Between 22-24 days, the lips of the neural groove fuse to form the neural tube
4. The notochord, under the neural tube is important in organizing the structure of the
brain. It sends chemical signals (Sonic hedgehog) that result in a chemical gradient
and differentiation into motor neurons.
5. The somites send chemical signals to guide the movement of cell outwards to form
the PNS. They eventually differentiate into the spine and ribs.
6. The cells of the neural crest break off and are the ones to migrate to form the
PNS. their exposure to different chemicals at different times is what causes them to
become different cells.
7. The sensory placodes arise next to the neural tube and the sensory organs arise
partly from those.
8. As the neural plate closes into the neural tube, constrictions appear dividing off
anlagen of forebrain, midbrain and hindbrain
9. Day 29, Rhombomeres form in hindbrain anlage: transient division in the hindbrain,
as many as 8 have been described.
10. Cell patterning: region-specific cell types are produced at predictable locations and
times with predictable patterns of migration and final positions. This works through a
3D grid of chemical signaling which allows for so little genes to form so many NS
cells
11. Cell-patterning is later fined-tuned by apoptosis but the original arrangement is highly
precise
7 developmental processes:
1. Neurogenesis
Production of new cells. Happens more in early life but keeps going until you die.
Progenitor cells in the ventricular zone migrate short distance to form the
subventricular zone by symmetrical division. They later divide through asymmetric
mitosis into radial glia and then into more precursor, neuroblasts and glioblasts.
Stem cells have not differentiated into neurons and glia yet. A stem cell can renew
itself into another stem cell or into a precursor cell which will then differentiate further.
Asymmetric mitosis: some proteins are pulled to one side of the cell before it
divides so that two new cells have the right components to differentiate
2. Migration
 Radial glia: extend temporary network of projections from ventricular zone to pial
surface to guide outward migration in CNS. acts as a scaffold on which cells will
“walk” to their location (CAMs, cell adhesion molecules, help guide the cells towards
heir position. Radial glia will differentiate into astrocytes when they’re done (only a
little remains).
a) Migration occurs in wave. First, the preplate zone is established by a wave of
migration from the ventricular zone.
b) The second wave migrates through the intermediate zone to split the preplate
into the marginal zone and the subplate.
c) Successive waves migrate out to expand the cortical plate, climbing atop
under the marginal zone one at a time. The subplate dies off by apoptosis
after this.
d) Additional migration from subcortical neurons and interneurons of cortex
*Focal cortical dysplasia occurs when the organization didn’t work properly. May be
a focus of epilepsy
3. Differentiation
Pluripotent precursor cells differentiate into non-dividing neuroblasts and glioblasts
that mature into specialized neuronal and glial cell types.
The remaining ventricular zone cells differentiate into ependymal cells, forming the
linings of the ventricles and spinal column.
4. Synaptogenesis
Extension and contraction of filopodial structures from the growth cone: specialized
swellings at the tip of axons and dendrites. The filopodia adheres to CAMs laid down
by other cells and pulls the growing axon behind it as it advances.
Chemoaffinity: postsynaptic target releases chemical label that attracts growing
axon (dissociated neurons can innervate appropriate targets in vitro, reversal of
chicken spinal cord)
Netrins: identified as chemoattractant (CAMs can also be chemorepellent such as
protein Slit)
Fasciculation: Once an axon has arrived at a certain site it climbs and follows the
axon of an existing cell to get to its final site
5. Apoptosis
Way too many cells are produced to account for the error rate. Cells that do not
contact their target undergo apoptosis. Neurotrophic factors are produced by
different cell groups and transmitted through innervation. This is a competitive
process and cells that do not get enough of them are likely to die off.
Cells shrink, chromatic condenses, cytoplasm and nucleus are phagocytized.
Phagocytosis is triggered by the surface expression of death signals. Immune
response is NOT elicited.
Chemically: Bcl-2 usually inhibits Diablo but when there’s a lack of growth factor
Bcl-2 is not expressed and Diablo is released. Diablo binds to IAPs which usually
inhibit caspases. Caspases activate endonucleases and breakdown of cytoskeleton.
*This can cause the death of cells around it because they don’t get the trophic factors
they need.
Necrosis: damage or infection of a cell so that it breaks open, and leaks outside.
Different from apoptosis where the cell will digest itself first. Immune response is
elicited and there can be brain damage.
6. Synaptic rearrangement
 Surviving neurons synapse on each other. Synaptic density peaks at about 1 year.
Topographic gradient: integrity of the neuronal map is maintained from source to
target, adjustments are made as source and target grow at different rates. Organized
by chemical gradients.
7. Myelination
Starts 24 weeks after conception. First in spinal cord, then hindbrain, midbrain and
forebrain. Intense phase of myelination right after birth. Development of grasping
reflex is associated with myelination.
Babinski reflex: when neurons are not fully myelinated (should not occur after 2
years of age)
Experience:
- Visual deprivation: fewer synapses and spines in the primary visual cortex, deficits
in depth and pattern perception (and vice-versa for visual enrichment, rat experiment)
- Monocular deprivation impairs organization of ocular dominance during the
sensitive period. After this, it won’t do much. The damage is pretty much irreversible
if during the sensitive period.
- Methylation: the addition of methyl groups to adenine or cytosine confers stable
decrease in gene expression as cells divide and differentiate
- Histone acetylation: determines how much of DNA is available for transcription and
how easy it is to access it. Epigenetics shows experience can affect biology such as
how much methylation/acetylation in rat’s brains.
Fragile X syndrome: CGG repeats cause methylation of FMR1 gene, silencing FMRP.
Blocks the normal pruning of synapses after birth, cause mental impairment and
characteristic physical appearance.
PKU: Absence of an enzyme that metabolizes phenylalanine, so it builds up in the brain and
becomes toxic. People have to avoid foods containing phenylalanine and will likely not get
mental impairment.
Fetal alcohol syndrome: when a mother drinks during pregnancy, causes mental and
behavioral impairment as well as characteristic facial structure. Alcohol is a teratogen
substance that induces fetal abnormalities when consumed during pregnancy).
Autism: impaired social interactions and language skills and interest in a narrow range of
activities. May be more likely due to pollution or other factors. Children are born with a bigger
brain than normal.
Down syndrome: third 21 chromosome causes mental impairment
Hippocampus: hippocampal formation atrophy is the most correlated measure with memory
impairment as we age.
Elevated stress, depression, Cushing’s disease contribute to atrophy
AAMI: Age Associated Memory Impairment.
- Varies from mild impairment to severe dementia
- Hard to measure because of all individual differences and other factors affecting
memory
- Long term memory and working memory declines, vocabulary does not
- NIMH criteria: memory performance on at least one measure at least one SD below
performance for healthy young adults
- Intellectual professions & education may be somewhat protective, as well as exercise
- Depression may contribute (when active)
- Tangles and amyloid plaques are identified (which could mean this is a precursor to
AD)
 - White matter lesions and AAMI correlated in old people
- Loss of estradiol in females (promotes growth & synapses in hypothalamus, cortex &
hippocampus)
- Oxidative damage and inflammatory responses correlated with AAMI.
Vascular or multi-infarct dementia: dead area of tissue associated with cognitive
impairment
Alzheimer’s disease:
- Most common form of age-associated dementia. 10% of pop over 65, 25% over 85.
- Starts with a loss of memory for recent events
- Progressive loss in declarative memory, meanings, language, paranoia, agitation,
delusions, etc. in end stage, patients often mute and severely disabled. Cannot tall
anymore because forget what happened 5 seconds ago.
Amyloid plaques:
- Amyloid Beta form plaques
- High prevalence of Amyloid-beta 42 and 40 that are highly prone to
aggregation
- Once a buildup forms, it tends to attract more plaques
- May be the result of an overly vigorous response to infection
TAU tangles:
- Overly phosphorylated TAU proteins
- Swollen soma and displaced nucleus
- Their prevalence is directly correlated with cognitive impairment, they may be
a response to amyloid plaques
Plaques and tangles are first restricted to the hippocampus and then spread. These
may cause the neurons in the basal forebrain to stop producing acetylcholine
- 3 genes mutations identified for early onset AD
- Increasing number of ApoE4 increase risk for late onset AD
Causes:
- 3 autosomal dominant gene mutations are identified for early onset AD,
affect processing of amyloid precursor protein
- late onset AD, apolipoprotein E gene on chr 19 is implicated.
- increasing number of copies of ApoE increases risk for late onset AD
(could be implicated in scavenging and clearing amyloid peptides from
extracellular space in brain)
Mental activity, exercise and sleep are protective no matter the genes.

Chapter 8 study guide

5 senses? This is challenged by our senses for:
- Pressure
- Temperature
- Pain
- Proprioception
- vestibular/balance (in the inner ear)
These a submodalities of somatosensation that we all put under the name “touch” event
though they come from different receptors and are integrated in different neural pathways.
Umwelt: species specific perceptual world.
Sensation: detection of stimulus and recognition that event has occurred
Perception: interpretation and appreciation of a sensory stimulus
Sensory salience: our brains have bigger regions for more important modalities. Ex. in
human a lot (more than half) is allotted to visual perception and in rats a lot is for olfactory
perception.
Specific Nerve Energies, Johannes Muller: hypothesized that each sensory pathway used
a different type of energy to stimulate the brain so that it know which is what. We now know
this is not the case. Rather, labeled lines is the fact that each sensory modality sends its
axons along different tracks (all using action potentials).
Sensory receptors: specialized neurons that detect specific physical stimuli. Most of them
do not have axons and their cell bodies synapse on dendrites or cell bodies of other
neurons.
3 stages of sensation:
1. Reception (stimulus to receptor, absorption of physical energy)
2. Transduction (receptor to neuron, conversion of physical energy to electrochemical
pattern in neurons)
3. Coding (neuron to brain, correspondence between some aspect of the physical
stimulus and action potentials)
Receptive fields help sharpen and define sensory inputs. Larger in less sensitive systems
and smaller in more sensitive systems. Comparing the input coming from many receptive
fields allows for perceiving movement and direction. Lateral inhibition sharpens the acuity
of sensory recognition.
Hierarchical processing: successive levels of processing extract more complex features of
a stimulus. Most sensory info goes through the thalamus, the primary sensory cortical area
and then the non primary sensory cortical areas.
Processing intensity:
- Which neurons are active
- Frequency of AP firing (but this is limited)
- Assemblies of neurons can act together so that intensity is encoded by how many
neurons are active
- Neurons can fractionate the range of intensity they respond to so that which
neurons are active indicates how intense a stimulus is
Processing frequency:
- Which neurons are active
- Number of APs in specific neurons (limited)
Processing location: somatosensory and visual maps in the brain tells us where a stimulus
is.
Tonic receptors: slow or no adaptation to stimulus
Phasic receptors: rapid adaptation to stimulus
Adaptation: can be achieved at the level of the sensory receptor or at higher levels of
processing. For instance, a pacinian corpuscle detects vibration, but prolonged vibration will
result in slower and slower rate of AP firing. If the vibration stops, then the corpuscle will fire
again. Can also be achieved through descending inputs, such as opioid analgesia. Sensory
systems emphasize change in stimuli, because this is more likely to be important for the
organism.
Plasticity: sensory processing can change depending on experience. The somatosensory
map can enlarge for a region that is used more that others (ex. Monkeys trained to touch a
disk with two fingers, musicians)
Epicritic touch: fine and discriminative touch, proprioception.
Mechanoreceptors:
 - Pacinian corpuscle: sudden, deep pressure, texture, adapts quickly
- Meissner corpuscle: sudden, light touch, adapt quickly
- Ruffini corpuscle: stretch of the skin, large receptive fields, adapt slowly
- Merkel’s disk: light/fine touch, inhibitory surround, slow adaptation
- Proprioceptors: muscle spindles, golgi tendon organs, joint proprioceptors
These all send their axons through the dorsal column system: they’ll go to the
medulla and then cross to the thalamus on the opposite side of the body, then primary
somatosensory cortex (S1).
Protopathic sensation: nondiscriminating, pain and temperature
- Free nerve endings, responsive to tissue damage, release of K+ from the nerve.
Transmits using C & Aalpha fibers.
- Ascending pain fibers release substance P (and others)
- Analgesia: mediated by descending projections from PAG, raphe, etc. mimics opiate
drugs.
These signals go through the spinothalamic tract: the difference is that it crosses to the
opposite side in the spinal cord before reaching the brain.
Pain receptors & control, social rejection:
- Nociceptors are specialized to respond to pain
- When initially activated, nociceptors use a particular type of voltage-gated sodium
channel to report pain
- Cannabis, opiates, spinal block are analgesic
- Surgery such as frontal lobotomy or cutting nerve cords can help but there is
significant risks that pain will return, or severe effects on behavior (lobotomy)
- Stimulation of the periaqueductal grey induces potent analgesia. Stimulates medulla,
which stimulates spinal cord and eventually endorphins are released at the source of
pain. Frontal cortex, cingulate cortex and hypothalamus can direct periaqueductal
grey to do this.
- Placebos can induce this release of opioids and somewhat relief pain (works better
when seems expensive, big pill and from a doctor)
- Stress can induce analgesia for some time (right after an injury someone may not
feel it until they’re out of danger)
- Social rejection activates the same pathways as physical pain
Heat and cold:
- TRP is a family of receptors that respond to heat/cold
- Capsaicin activates those, which makes us feel like pepper is hot
Thalamus: relays sensory information through appropriate circuits

Chapter 10 study guide

Visible Light: The light we see is only a small portion of the electromagnetic spectrum
(380-760 nm wavelengths). Other animals with different umwelts may see ultraviolet (bees)
or other wavelengths.
Color/hue: is encoded by wavelength/frequency
Purity/saturation: a light containing all wavelengths in equal amounts will appear white. A
light containing only 1 wavelength will be saturated, a very pure color. A light with a mix of
wavelengths will appear as the dominant wavelength(s).
Brightness: magnitude or intensity of waves determines this perception
Vergence movements: foveating on a target, both eyes on it. Can be either divergence or
convergence movements depending on if an object is far or near.
Saccadic movements: scanning a room, for instance, the eye abruptly shifts from one point
to another
Pursuit movements: smooth tracking movements that keep object’s image fixed in place on
fovea
Human eye:
- Dilation is mediated by the sympathetic NS while constriction is mediated by the
parasympathetic NS
- Fovea only contains cones, acuity and color perception (in the dark you see better in
the periphery). Also has less blood vessels and layers of cells on top of it so more
light reaches it
- High density of rods outside the fovea (spatial summation in low light with the loss of
precision and details)
- Light is focused on retina by lens (ciliary muscles) and cornea (fixed curvature)
- Photoreceptors are at the back of the retina: 120,000,000 rods 6,000,000 cones
- Cones (Photopic): low sensitivity, low convergence, small receptive fields in fovea
and larger in rest of the eye
- Rods (Scotopic): high sensitivity, high convergence circuits, large receptive fields
- Optic disk: where the nerve connects from the eye to the brain, contains no
photoreceptors so is a blind spot. We are usually not aware of it because our brain
can fill in the missing information based on the other things around it
- Layers:
a) Ganglion cells LAYER
b) Amacrine cells (interneurons): contact bipolar and ganglion cells, may play a
role in direction selectivity, on-off
c) Bipolar cells LAYER
d) Horizontal cells (interneurons): contact photoreceptors and bipolar cells,
help with lateral feedback inhibition and help increase contrast and edges.
Releases GABA which hyperpolarizes bipolar cells & inhibits ganglion cells.
e) Photoreceptors LAYER
Photoreceptors: contain several hundred lamellae (thin membrane plates), which each
contain millions of molecules of photopigment. These molecules consist of opsin and 11-cis
retinal. Rods contain rhodopsin and cones contain iodopsin - these opsins are broken down
by the energy from a photon of light. At rest (in the dark), photoreceptors are continuously
releasing glutamate. When photon hits photoreceptors, the broken molecules of rhodopsin,
iodopsin or melanopsin interact with G-proteins (transducins) and close the Na+ channels.
This hyperpolarizes the cell and the photoreceptor stops releasing glutamate.
Photoreceptors synapse on bipolar cells, which synapse on ganglion cells. The axons of
ganglion cells meet to form the optic nerve. Cells that are farther from the optic disk have
higher conduction speeds so that their inputs arrive at the same time as proximal cells’.
Photoreceptors and bipolar cells produce only graded potentials while ganglion cells produce
action potentials.
Convergence of information: although there are about 104 million photoreceptors, there
are only around 1 million ganglion cells. The information converges and that is transmitted to
the brain.
Optic chiasm: optic nerves join at the ventral aspect of the brain to form X-shaped optic
chiasm. The middle of the visual field goes to both eyes while the right side of the visual field
crosses to go to the left side of the brain and vice-versa. After the optic chiasm, the nerves
go to the dorsal lateral geniculate nucleus of the thalamus, which send its axons to the
primary visual (striate) cortex.
Receptive fields bipolar & RGCs:
- Light always hyperpolarizes photoreceptors but it can either hyperpolarize or
depolarize bipolar cells. Bipolar cells also release glutamate, which always
depolarizes retinal ganglion cells.
- On-center bipolar cells: when light hits the center of their receptive field, they get
excited because they receive less glutamate (glutamate inhibits them)
- Off-center bipolar cells: when the light is turned off at the center of their receptive
fields, they get excited by receiving more glutamate, which depolarizes the cell.
- When communicating to ganglion cells, on-center cells will excite (depolarize) the
cells when the light is on and off-center will excite the cell when the light is off.
- On-center-off-surround receptive fields of RGCs excite the cell when the light is on
the center of the field and inhibit it when it’s on the outside ring on the field.
Off-center-on-surround cells respond in the opposite way. Uniform light across the
field results in little change in polarization of the bipolar cell and firing rate of APs of
the ganglion cell connected to it
ON/OFF cells are excited briefly when light intensity changes anywhere in their
receptive field. Project primarily to superior colliculus and do not play a direct role in
object perception.
Coding of light and dark:
- Overlapping receptive fields provide color enhancement
- From bipolar cells onward in primary visual system, cells respond better to spatial or
temporal contrast than to absolute light levels (Mach Bands illusion)
Color coding:
● Evolved for ripeness, counteracting camouflage
● Humans, old world monkeys and apes each have 3 types of cones (iodopsin) -
SECOND most elaborate color vision in the animal kingdom (after the mantis shrimp,
which has 16 types on cones)
● Trichromatic theory of color vision: based on the theory that we can obtain any color
by mixing yellow, red and blue. Hypothesized that we have 3 types of photoreceptors
that work together to give perception of color.
● Cones: 3 types with a different iodopsin & a different maximal response
○ 440 (short)
○ 530 (medium)
○ 560 (long)
● Opponent process theory of color vision: based upon the idea that some colors
don’t blend, and upon negative afterimages. Staring at a certain color fatigues a type
of cone so an afterimage appears when looking somewhere else - the cone cannot
process that color at all atm.
○ 2 kinds of opponent color sensitivities in ganglion cells:
■ Medium opposes Long (L-on/m-off or L-off-M-on)
■ Short opposes Medium/Long (S-on/L+M-off)
■ For instance: green (medium) excites M-on/L-off and inhibits
M-off/L-on, somehow inhibits S-on/L+M-off
Types of ganglion cells
1. Parvocellular (midget cell)
- Small cell bodies, small receptive fields
 - Mostly in fovea
- Sensitive to color and detail
- Synapses on parvocellular cells of LGN
- Ventral Stream, “what” pathway: color vision, identifying forms and features
of objects. Occipito-temporal, inferior-temporal and inferior frontal cortex.
- Recognition becomes more complex at higher (more frontal) levels
- Posterior = general info about facial features, gender, etc.
- Anterior = recognition of individual faces
- Fusiform cortex: facial recognition
- Extrastriate body area: body parts
2. Magnocellular cell (parasol cell)
- Larger cell bodies and receptive fields
- Throughout retina
- Responds best to moving stimuli
- Brightness and depth perception
- Synapses on magnocellular cells of LGN
- Dorsal Stream, “where” pathway: important for spatial location, organizing
movement towards objects.
- Occipito-parietal, parietal cortex
- Motion detection: Area MST. Stabilizes visual image by comparing
relative movement of objects in visual field. Important for when we’re
moving and objects around us are static. MSTd is important for optic
flow.
3. Bistratified cells
- 8-10% of ganglion cells
- Inputs from rods, cones and amacrine cells
- Synapse on koniocellular cells of LGN (info about short wavelength cones)
4. Photosensitive RGNs
- 1-3% of ganglion cells
- Giant cells containing melanopsin
- Sluggish, long-term responses
- Contribute to synchronization of daily rhythms, regulation of pupillary
constriction
LGN
- In the thalamus
- 6 layers: the 4 dorsal ones are parvocellular (small receptive fields, color processing)
while the 2 ventral-most ones are magnocellular (bigger receptive fields, no color
processing, orientation and movement information)
- Layer 1, 4 and 6 process information from the opposite eye and layer 2,3,5 from the
same eye (all from the opposing visual field)
- The LGN functions as a topographically organized relay station and provides
topographically-organized input to PVC, known as retinotopic organization
Retinotopic organization
About half of V1 is devoted to the foveal region, allowing for great acuity there.
Additional visual pathways:
1. Retinogeniculocortical pathway (retina, LGN, V1) 50% of primate cortex is implicated
in visual processing and associated functions
 2. Retino-tectal pathway organizes coordinates eye movements, control of the muscles
of the iris (pupil size) and control of ciliary muscles (lens shape for focus)
3. Retino-suprachaismatic-hypothalamic pathway synchronizes diurnal activity cycles
Primary visual (striate) cortex (V1)
Represents 4 aspects of visual stimulus:
1. Location in the field
2. Color
3. Ocular dominance (most cells are binocular but respond more strongly for one eye)
4. Orientation
Cortical columns: receptive fields of all cell in a column have roughly the same retinotopic
location, and these locations change systematically in nearby cells.
- Parvocellular circuits carry inputs from medium and long wavelength cones
- Koniocellular circuits carry inputs from short wavelength cones
- Magnocellular input to V1 provides info about orientation and movement.
V1: where input comes first, very stimulated by color. Interblolb region of V1: input to
thick striped to provide info about ocular dominance, orientation, movement. Each interblob
column has similar response properties but it changes systematically across columns.
- Some cells respond maximally to a vertical/horizontal/oblique line
- All orientation sensitive cells have tuning curves - orientation sensitivity changes
smoothly through a rotation with larger jumps sometimes
Simple cells: orientation-selective receptive fields, found in layer 4. Receive input from
LGN.
Complex cells: orientation selective tuning that has no center/surround organization. In
layers 2 & 3 and mostly receive input from layer 4. Receive input from rows of simple cells.
V2: respond to differing to represent corners
V4: rich in color-sensitive cells, color constancy
V5: simple motion and direction analyzed. Cells respond specifically to movement, in
a specific direction, specific speed. Opponent process.
Spatial-frequency filter Model: Contrast between lighter and darker parts of visual stimulus
as eyes move yield patterns of spatial frequency, including high and low frequency aspects.
High frequencies give us details, while low frequency give large uniform areas and gradual
transitions
Depth perception:
- Combination of monocular and binocular cues
- Monocular cues:
- Perspective
- Relative retinal size
- Loss of detail in distance
- Relative apparent movement as you move head
- Binocular cues:
- Retinal disparity
Prosopagnosia: inability to recognize faces
Damage:
● To the ventral stream: difficulty identifying objects or faces
● To the dorsal stream: ability to identify objects but difficulty reaching for them
Columns (V1):
- Ocular dominance columns: all the cells in a column have the same ocular
dominance, this is especially salient in area V4, where cells respond to 1 eye only
 - Columns may also be tuned to a specific orientation (ex. 10 degrees)
- Some columns are tuned to a specific spatial frequency
Blobs:
- Blobs were discovered through cytochrome oxidase stains
- In the primary visual cortex, mostly layer 2,3 but also 4.5.6
- Regions (similar to columns) that are sensitive to color - receive input from cones
- Interblob regions are sensitive to motion and spatial frequency and receive input from
both the retina and the blobs, suggesting they’re involved in higher level processing

Chapter 11 Study Guide

Motor plan: Complex set of motor commands to muscle that is established before the
behavior starts, and refined as it unfolds (closed-loop system). This is in contrast to
Sherrington’s idea that all behavior is simply reflexes
Motor unit = smallest unit of motor activity
- For instance, an alpha-motor neuron and the myofibers it innervates
- Slow motor units are used in continuous effort
- Fast motor units = 2 subtypes, used in fast movements
- Fewer fiber per axon = more precise control (small recruitment = more precision)
- Ex. eye muscles have very low innervation ratio while a leg muscle has a high
innervation ratio
Motor pool = all motor neurons that innervate the fibers of a single muscle
Closed-loop system: A system where the information flows back to the device and can be
tweaked as it unfolds. Maximizes accuracy.
- Has a transducer, an error detector, a controller.
Open-loop system (ballistic movements): This system maximizes speed and there is no
possibility to correct action once it’s done. For instance, throwing a ball.
Has only the transducer communicating to the controller with no feedback.
Both systems involve the primary motor cortex, nonprimary motor cortex,
brainstem, spinal cord and then the muscles of the body. In closed-loop systems, the brain
also analyzes sensory inputs, basal ganglia modulation and cerebellar modulation that
permits real-time adaptation.
Central patterns generators: neural circuitry responsible for generating rhythmic patterns
of behavior, such as walking. Initiated and modulated by the brain, fine-tuned by sensory
input. Polysynaptic flexor activity couple w ipsilateral extensor relaxation
Proprioception: Perception of body movements and position
1) Muscle spindles - monitor muscles length
Cylinder containing muscle fibers: intrafusal fibers connected to spindle afferent
neurons (sensory) and gamma motor neurons (motor). Gamma motor neurons contain
intrafusal fibers to regulate sensitivity of muscle spindles to contraction of surrounding
extrafusal fibers. The latter are innervated by alpha motor neurons, contraction supplies
muscle force.
- Primary sensory endings are wrapped around the middle of the spindle. Respond
early in stretch and adapt (phasic response). Communicate velocity of muscle stretch
- Secondary sensory endings are towards the ends and maximally sensitive to
maintained muscle length, a tonic response. Communicate muscle length.
- Gamma motor neurons alter the tension on the spindle so that it stays sensitive
Monosynaptic stretch reflex: a muscle is stretched, the sensory nerve inputs to the
spinal cord and the spinal cord directly input back to surrounding muscle fibers
 eliciting a reflexive contraction. Ex. the (patellar) knee jerk reflex is a monosynaptic
reflex.
- Alpha motor neurons: Sending command to the alpha motor neurons is the final
step in moving your muscles (contraction). The more action potentials, the more
movement
2) Golgi tendons - monitor muscle tension
In the tendon (attach muscle to bones). Not very sensitive to stretch but sensitive to
load/contraction. Acts as a brake to prevent overly vigorous contractions/tearing a
muscle. The tendon is pulled by muscle contractions, which activates the GTO.
Polysynaptic reflex: sensory nerve feeds back to excite spinal inhibitory
interneuron. Interneuron inhibits alpha motor neurons to diminish contractile force. 2
synapses, not as fast/direct as monosynaptic reflexes. Spinal cord also sends
messages to higher levels of CNS.
● Field sobriety test tests proprioception
2 classes of proprioceptors:
- Joint proprioceptors
1. Type 1
- Located in the fibrous joint capsule
- Continuous discharge that varies with limb position
- Maximal discharge at “best position”
2. Type 2
- In fibrous joint capsule
- Adapt rapidly
- Maximally activated by rapid movement
- Function to detect movement and acceleration
3. Type 3
- Along ligaments
- High threshold and slow adaptation
- Unknown function, perhaps protective reflexes
4. Type 4
- Fine unmyelinated fibers throughout the joints
- May play a role in joint pain
- Signal movements of joint at extremes of flexion & extension
- Muscle/tendon proprioceptors
Neuromuscular junction: cholinergic synapse between motor neurons terminal and muscle
fiber membrane
Motor end plate: point on the muscle fiber at which the synapse occurs (neuromuscular
junction)
End plate potential: - A single action potential in motor neuron produces very large
depolarization of postsynaptic membrane (much larger than typical EPSPs)
- Reliably initiates action potential in myofiber
- AP propagates along the length of the myofiber (both ways)
- Axon terminal releases acetylcholine.
- Nicotinic receptors open cation channels.
- Cation influx depolarizes endplate
- Voltage-gated Na+ channels open
- APs propagates in both directions
Differences between CNS synapses and neuromuscular junction:
 - NMJ propagates in both direction, only excitatory, acts for each AP rather than
needing summation
- CNS synapse can be inhibitory or excitatory
- Inhibition can only occur through CNS through IPSPs
Muscle contraction:
1. Skeletal muscles are made of many myofibers. Each myofiber is made of many
myofibrils
2. Myofibrils composed of actin and myosin filaments, arranged in repeating
sarcomeres.
3. In a striated muscle, the myosin and actin overlap. Contraction of the muscle
increases the overlap, shortening the muscle fiber.
Synergist & Antagonists: Around a joint, muscles are arranged in a reciprocal fashion;
when one muscle group contracts, it stretches the other one. Muscles that contract together
are called synergists, muscles that contract while the other stretches are called antagonists.
Movement around a joint requires one set of neurons to be excited while the other set is
inhibited. Activation of flexor causes inhibition of extensor (vice-versa, ea.withdrawal reflex)
Contraction of flexor muscle produces limb flexion. Contraction of extensor muscle
produces limb extension. Ex. bicep = flexor tricep = extensor
Primary motor cortex (M1):
- Precentral gyrus
- Homunculus (somatotopic organization)
- Disproportionately large regions for fingers and musculature used for speech in
humans
- Organization of M1 far less discrete than previously thought - regions somewhat
overlap so that movements can be seamlessly coordinated
- In monkeys: brief stimulation causes brief jerky movement, prolonged stimulation
caused complex movement. Many cells respond to specific muscle contractions but
many more cells respond to particular patterns of movement.
- Intention starts at the prefrontal cortex, the sequence of movement is largely
premotor and supplemental cortices, actual behavior is mediated by the primary
motor cortex
- Directional tuning: many M1 cells change their firing rate in relation to movement
commands, mediating direction of movement
- Plasticity here as well, somatosensory map can grow when learning a skill
Prefrontal cortex:
- Receives sensory input from the temporal lobe (visual/auditory). Sensory inputs from
parietal lobe (spatial orientation). Important for sensory-motor integration
- In the prefrontal cortex, instead of going from basic processing to abstraction like in
the visual cortices, it goes from abstraction to simple motor commands.
Premotor cortex & Supplementary motor area (nonprimary motor cortex):
- Input from prefrontal cortex, parietal & temporal cortices
- Output to primary motor cortex
- Important in planning complex sequences of behavior
- Supplementary motor cortex: initiates and organizes complex sequences of action
- Bilateral supplementary motor cortex lesion impairs initiation of voluntary motor
behavior
- Premotor cortex: what you’ve learned to do, communicating what exact movements
need to be done
 - Premotor cortex lesion impairs stance, gait, limb coordination but fine motor function
is spared
- F5: sensation and movement combine
Mirror neurons: In F5 (premotor cortex), these neurons fire when monkeys are doing a
behavior but also whenever they see a human do the same thing. Involved in interpretation
of intentions, learning, maybe in autism.
Basal Ganglia: inhibitory output to prefrontal cortex and brainstem, planning and production
of movement, inhibition of excess activity. The basal ganglia receives input from the cortex,
to the thalamus and back to the cortex, forming a loop.
- Striatum = caudate and putamen (CPu): caudate refines movement. Receives
output from cortex and thalamus, mostly excitatory.
- Subthalamic nucleus (STN): receives output from cortex and thalamus, mostly
excitatory.
- Globus pallidus: receives mostly inhibitory outputs from striatum and mostly
excitatory outputs from STN
- Substantia Nigra
1. Direct pathway: Loop (2 inhibitory links) activate cortex and facilitates
movement
2. Indirect pathway: Loop (3 inhibitory links) inhibits cortex and suppresses
movement
3. Hyperdirect pathway: Loop (1 inhibitory link) inhibits cortex and suppresses
movement
- Balance of the 3 pathways regulates expression of motor behavior

Cerebellum:
- 50 billion out of 86 billion neurons are in the cerebellum
- Receives sensory input from all modalities
- Medial cerebellum controls ventromedial tracts (posture) while lateral cerebellum
controls lateral tracts (independent skilled limb movements)
- Input to the cerebellum provide info for motor function while its output influences
motor systems
Lobes:
1. Flocculonodular lobe - vestibulocerebellum
Implicated in balance, eye movements
2. Posterior lobe - cerebrocerebellum
Voluntary activity, procedural memory
3. Anterior lobe - spinocerebellum
Gait (démarche), coordination, skilled movements
Longitudinal zones: Extend projections to 3 deep cerebellar nuclei
- Medial zone (vermis): vestibular, visual, auditory, somatosensory inputs. Regulates
posture, gait. Projects to vestibular (brainstem) & spinal cord.
- Intermediate zone: receives motor commands from motor cortices, and
somatosensory (limbs). Regulates limb movements, independent of trunk. Projects to
thalamus and red nucleus (brainstem)
- Lateral zone: receives cortical, pontine inputs, motor commands, somatosensory
info from spinal cord. Regulate independent limb movements to accomplish rapid
skilled movements that require precise timing (ballistic movements). Projects to
dentate nucleus, thalamus and red nucleus (brainstem).
Descending tracts:
Lateral Tracts:
- Input from M1
- Independent movements of distal portion of limbs
1. Pyramidal tract
- In finger, hand, arm regions of M1 (controls those)
- Grasping and manipulation
- Terminate in spinal cord
2. Corticorubral-rubrospinal tract
- Originate in M1 and red nucleus (brainstem)
- Terminate in spinal cord
- Controls hands (not fingers), feet, distal portion of limbs
3. Corticobulbar tract
- Originate in face region of M1
- Terminates in cranial nuclei
- Control face and tongue movement
Ventromedial tracts:
- Inputs from midbrain/brainstem nuclei and from M1
- Mostly control of trunk and proximal portions of limbs
1. Ventral corticospinal tract
- Originate in trunk and proximal region of M1
- Terminate in spinal cord
- Controls trunk, legs, feet
- Walking and posture
2. Vestibulospinal tract
- Originate in brainstem vestibular nuclei
- Terminate in spinal cord
- Controls trunk and legs, posture
3. Tectospinal tract
- Originate in superior colliculi
- Terminate in spinal cord
- Controls neck and trunk
- Coordinate eye/head movements
4. Lateral reticulospinal tract
- Originate in medullary reticular formation
- Terminate in spinal cord
- Controls flexor muscles of legs, walking
5. Medial reticulospinal tract
- Originate in pontine reticular formation
- Terminate in spinal cord
- Controls extensor muscles of legs, walking
DISORDERS
Myasthenia Gravis:
- Neuromuscular junction don’t work, muscles don’t get the message to contract
- Autoimmune disorder: antibodies attack a patient’s ACh receptors
- First muscle of the head: drooping of the eyelids, double vision, slow speech. Later
stages result in paralysis of the muscles that control swallowing and respiration and
is life-threatening
 - Treatment: suppressing the immune system, AChE inhibitors
Multiple sclerosis:
- Disease of CNS myelin, gradual destruction of myelin sheaths
- Autoimmune dysfunction
- Accompanying development of hard scar tissue
- Later stages: muscular weakness, tremor, urinary incontinence, numbness, visual
disturbances, ataxia (trouble in balance and walking)
- Onset in early adulthood
- Occasional remissions
Amyotrophic lateral sclerosis - ALS (Lou Gehrig’s disease)
- Rapid, progressive atrophy of CNS and PNS motor neurons (brain and spinal cord)
- Onset between 40-70
- Death usually in 2-5 years
- No dementia
- Eyes and bladder spared
- Advanced ALS: progressive weakness, paralysis, wasting of muscles, loss of
speech/swallowing/breathing
- Causes not clearly established. 10% arise from a single gene defect in superoxide
dismutase gene. Other causes may be toxic mineral exposure, immune responses,
endocrine dysfunction
Cerebellar ataxia:
- Cerebellar disease/damage causing ataxia, astasia (inability to stand upright)
intention tremor
- Loss of coordination of the legs
Apraxia:
- Inability to carry out complex movements even if paralysis or weakness is not evident
and language/motivation are intact
- Can still do things like smile but cannot do it when asked to
- Ideomotor apraxia: incorrect organization or sequencing of movement, left frontal or
parietal lesions
- Constructional apraxia: skilled movements are intact but inability to draw or
assemble, right parietal damage
Parkinson’s disease:
- Destruction of dopaminergic cells of SNpc (which project to caudate nucleus,
regulation of excess movement)
- More than 70% of dopaminergic neurons are destroyed before first symptoms
- Symptoms: tremor, rigidity, slow movement/inability of movement, postural instability
- Later stages: loss of voluntary behavior and death
- Depression and dementia
- Stages:
1. Symptoms on one side, inconvenient but not disabling, tremor of one limb,
changes in posture and facial expression
2. Bilateral symptoms, posture and gait affected
3. Slowing of body movements, impairment of equilibrium, generalized
dysfunction, constant nursing care required
4. Severe symptoms, can still walk a little, not able to live alone, maybe less
tremor than before
 5. Cachetctic (loss of body weight and muscle mass), complete invalidism,
cannot stand or walk, constant care needed
- Cause unknown, but associated with toxic insults, disease
- Treatments:
- L-dopa + carbidopa (converted to dopamine)
- Bromocriptine (dopamine receptor agonist)
- Selegiline (MAO-B inhibitor)
- Amantidine (increases dopamine release and blocks reuptake)
- Benztropine (antagonizes muscarinic cholinergic receptors)
- Diphenhydramine (benadryl) (antagonizes muscarinic cholinergic receptors,
may block dopamine reuptake)
- Surgery: fetal nigra cell grafts, pallidotomy, deep brain stimulation
Huntington’s disease:
- Autosomal dominant disorder that onsets in early middle-age (35-50 years)
- Loss of striatal neurons, atrophy of caudate, decrease in GABA and substance P
- Jerky movements and intellectual deterioration, facial grimacing, ataxia
- Later stages, muscular rigidity occurs
- Psychiatric disturbances, apathy & irritability, manic-depressive, schizophrenia
- Walking, swallowing, dementia disables severely in later stages
- No treatment known for this progressive disorder, genetic counseling is important as
½ of offsprings will be affected