Neurobiology Lectures

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How does postsynaptic inhibition work? (what channels): Causes opening of K and Cl receptors that make the iside fo the cell membrane more negative (hyperpolarized)
What point on the nerve cell has the lowest AP threshhold?: Axon hillock
How can you bias the excitability of a neuron?: Change the tonic (baseline) level of excitation or inhibition (often pharmacologically)
Name several classes and examples of CNS neurotransmitters: 1) amino acids (glutamate, glycine, GABA)
2) Neuropeptides (Substance P, CGRP, somatostatin)
3) monoamines (epinephrine, norepinephrine, dopamine, seratonin)
4) other small molecules (histamine, ATP)
Glutamate: excit or inhib?: excit
glycine: excit or inhib"?: Inhib
GABA: excit or inhib?: Inhib
What class/kind of receptor is the ACh receptor in the NMJ?: Ionotropic--the receptor itself is an ion channel
Another name for ionotropic receptors: ligand gated ion channels
How long do ionotropic channels stay open when active?: Short active: milliseconds
Describe metabotropic receptors: Ion channel is a second molecule from receptor. Communication typically mediated by G-protein associated with the receptor.
Which neurotransmitters are associated with metabotropic receptors?: dopamine, epi, norepi, and the neuropeptides
What lenght of effect for metabotropic receptors?: Postsynaptic effects can last a long time--minutes to hours
What are the 2 kinds of glutamate receptors?: AMPA receptors
NMDA receptors

(based on which glutamate-like molecule can serve as an agonist for the receptor)
Can glutaminergic synapses have more than one kind of gluatamate receptor?: Yes. Can have NMDA and AMPA.
Are NMDA and AMPA excitatory or inhibitory?: Excitatory
What class of receptor is the AMPA receptor?: Ionotropic
What ions flow when AMPA receptor is active? What does this cause?: NA and K.

Causes a postsynaptic depolarization for 10-200 milliseconds
Generally, how does AMPA receptor work?: Like ACh receptor. AMPA binds receptor, causes Na and K to flow through ion channel in the recptor.
Generally, how does the NMDA receptor work?: 1) Co-agonist (gly or d-ser) must be present
2) Mg ion blocks the channel when membrane at rmp
3) When membrane is depolarized (by AMPA or otherwise), Mg is dislosged.
4) This allows CA and NA to enter.
5) this depolarizes cell further and leads to other downstream biochemical events.
Describe length of action of NMDA receptor: Downstream effects of this channel opening results in LONG LASTING increase in excitability.

can last HOURS or DAYS

Called LPP (LONG TERM POTENTIATION)
Describe current thinking about the nature of LTP: 1) it is a postsynaptic process
2) During LTP, AMPA receptors are added to the postsynaptic membrane (or silent AMPA-R are activated)
3) May also be a modification of the AMPA receptor/channel to increase ion conductance
What is the indispensible condition for LTP?: Depolarizatoin of the postsynaptic membrane sufficient to dislodge the Mg++ ion.
Describe the Activate-Test Different Pathways experiment.: If you tetanize dendrite at point 1 for ten seconds, you can get NMDA activation at a distant pathway 2 on the same dendrite as well. That is, pathway 2 elicits a larger respoones in testing even though it was not the one tetanized.

Why? Depolarization produced at pathway 1 depolarizes the membrane sufficiently even distantly to dislodge the Mg ion and cause LTP to occur (AMPA upregulation, making it easier to fire an AP)
How might actual Learning (which lasts years) occur?: In neurons undergoing LTP, there might be changes in protein folding within the cell or in those synapses, in a prion like domain. Leads to more permanent changes.
What is LTD?: Long term depreession. Seen when presynaptic axon is stimulated once per second or so. This REDUCES LTP.
Describe bad effects of glutamate: Too much around the nuerons can be neurotoxic.

How? It increases Ca conductance too much, which allows in too much Ca and is toxic to the cell.

This can be a problem in neuro trauma, in which a lot of glutamate escapes from cells into the extracellular space.

Some effort to develop drugs to reduce neurotoxicity of freed glutamate immediately following a stroke.
What does broca's lesion cause?: expressive aphasia
What does Wernicke's lesion cause: receptive aphasia
What does Broca's aphasia SOUND like?: Sparse, labored speech
Small grammatical wiords omitted
Deficit in writing and in speech
Comprehension intact
What side is broca's usually on?: Left (in R handed people. Leftys sometimes can have it on the right.)
Describe what Wernicke's defect SOUNDS like: Normal speech rhythm
Nonsensical
No comprehension of written or spoken word
What connects Wernicke's and Broca's area: Arcuate Fasciculus
Describe arcuate fasciculus lesion: Rapid, nonsensical speech
But with COGNITION, because wernickes is intact, so it can process and send signals to braiin about what it is hearing. but when signal comes back down to wernickes to then travel to broca's for expression (via the arcuate fasciculus), it transmits static, so broca's spits out nonsense.
What makes you male?: Sex determining region on Y chromosome.

Leads to production of testis dtermining factor, and development of testis. This leads to making of testosterone and making of MULLERIAN DUCT INHIBITING SUBSTANCE (MIS).
Describe androgen insensitivity syndrome: 1) XY genotype
2) Make testes
3) But receptors in body do not respond to testosterone
4) External phenotype thus looks female, though person genotypicaly male.
What did the gay brain study show?: nuclei in the Hypothalamus (INAH 3) were smaller in gay men (and more sized like women's) than in hetero men.
What is the planium temporale related to?: Perfect pitch.

Area of left planium temporale is larger in people with perfect pitch.

BUT: people never have perfect pitch unless they ALSO have musical training before age 7.
What are the classes of memory, based on duration and capacity?: 1) sensory memory
2) working (short-term) memory
3) Long term memory
Describe capacity/length of sensory memory: Large capacity.

Sensory memories vivid for a fraction of a second and then fade.
What is it called when sensory memory persists?: Eidetic imagery
What is the length/capacity of working memory?: Only 6-7 items at a time

Each stored for just a few seconds
Long term memory length and capacity: Seems virtually unlimited in capacity and duration
What is consolidation?: The process whereby certain items from sensory memory progress through working/short term memory on into long term memory
Name the categories of memory based on QUALITY: 1) declarative memory: knowing WHAT. Facts, experiences.

2) Non-declarative memory. Knowing HOW. MOtor skills, spatial memory, logical reasoning.

DECLARATIVE memory is most often affected in HUMAN pathologies.
What brain region is implicated in learinign in humans and animals?: Hippocampus
Where is LTP found?: hippocampus
What does APV do?: It is a selective NMDA receptor blocker, so it blocks LTP mechanism.
What happens when you give mice APV and have them do hidden platform test?: Reduces their ability to perform hidden platform test.
What happens when you knockout entire NMDA receptor complex gene?: inviable mice
What happens when you knock out biochemical pathways that are downstream of only the NMDA receptor?: diminished hidden platform performance.
What happens when you knockout only NMDA pathways in the CA1 region of the hippocampus?: Learinign is DIMINISHED, but they still can learn where the platform is. So this is involved but not everything.
What happens when you augment NMDA receptor conductance?: You can IMPROVE mice learning!
Is NMDA receptor in hippocampus specific to a type of learning?: Yes. Specific to PLACE learning (hidden platform). But doesn't seem to affect ASSOCIATIVE learning.
What did R.B. lose when he had lesion in CA1 region of hippocampus?: Seemed to lack ability to CONSOLIDATE working memory to long term memory. His existing long term memory was ok, and he had fine working memory. but he couldnt make new long term memories.

His NON-decalarative learning, howerver, was intact (could learn motor skills, spatial skills). His DECLARATIVE learnign of facts was deficient.
So what is the difference in hippocampal impairment in mice and humans?: In mice, it affects NON-declarative learning (place learning).

In humans, it does not affect nondeclarative, but it affects declarative.
Describe the third generation knockout experiment wiith mice and learning: They had inducible NMDA knockouts (NMDA turned off when fed doxy)

Group fed doxycycline in the consolidation interval (between learning time and retesting) had less retention.

If they got doxy AFTER the consolidation window, then it didn't affect retention
What are the main points of all of the consolidation experiments?: 1) You need NMDA receptors active DURING learning to learn.

2) but you ALSO need NMDA active during a discrete CONSOLIDATINON period after the learnign.
Name 3 ways to promote Consolidation of learning: 1) Visceral learning (bait shyness)
2) emotional learning
3) Working for a distant goal
Describe gist of emotional learning: Emotionally traumatic event can produce an eidetic image (long-term sensory image)
How can you simulate emotional learning: Right after training, give epinephrine, which stimulates b-adrenergic receptors that would be stimulated by afferents that would be active in emotional situation
What does propranolol do?: It blocks b-adrenergic receptors, and can impair memory formation in humans
What brain region is thought to be involved in emotional experience?: Ventromedial frontal cortex
What does lesion to ventromedial frontal cortex seem to cause?: All of your cognition and learning can be fine. But you can't FEEL. Emotional deficit. So without emotion, you can't work toward a long term goal, and you lose that important route of learning.

So separating emotion from other cognitive function may be a bad thing. The dude with this problem coudlt hold a job, keep wife or make investments
What kind of tests do people with ventromedial frontal lobe lesions perform poorly on?: Any learnign task that requires focus on an ultimate goal rather than short term gain.

They may even be able to intellectually articulate what the best long term strategy is, but in real life they have a hard time choosing it.
What mediates the absolute luminance threshhold for vision?: Rods. So lowest light vision is black and white.
Define sensory transduction.: The conversion of physical information associated with a sensory modality to electrical activity that represents that information
Define phototransduction: Conversion of light information in the visual system to electrical activity
What happens in retinosa pigmentosa?: Misfolded opsin protein

Opsin in outer cone segments cannot transduce light info.

No vision fro that cone.
What is the concentration (relatively) of rods and cones in the fovea?: Almost all cones, almost no rods
Note size of cones in fovea?: More cones in fovea, but size of them also is smaller so closer packing and greater overall number.
What is the spatial receptive field of a ganglion?: The region of a VISUAL FIELD where light can elicit an AP response from that retinal ganglion cell
How many rods might converge onto a peripheral retinal gangion cell?: 1500
How many cones might converge onto a fovea retinal ganglion cell?: closer to 1:1
What are P-cells?: Ganglia specific for form and color.
Small receptive fields
Either off or on center
Brisk and sustained responses to light
Important for color and acuity
What are M cells?: Bigger than P, more and wider dendrites
Larger spatial receptive field
Creates fast, transient responses--so more attuned to responding to Moving stimuli
What are paralell pathways?: Division of representation of distinct aspects of a sensory stimulus (e.g., form vs. motion) within distinct cells and circuits
Where do P cells relay into to?: Layers 3-6 of LGN

(3, 5 ipsilateral
4, 6 contralateral)
Where do M cells relay information to?: layers 1 and 2 of LGN

1: contralateral
2: ipsilateral eye info
How many layers are in the cortex?: VI
Which cortical layer receives input from LGN?: Layer IV
Which layer of primary visual cortex (V1) receives input from LGN?: Layer 4
Whate kind of receptive fields to neurons in layer 4 of V1 have?: Center/surround
What are ocular dominance stripes?: When you inject eyeballl with tracer and it is taken up by optic nerve, then you see discrete banding in layer 4 of V1, indicating there is segregation of the nerve pathways for each eye in this layer.
Is eye info segregated in layers 2/3 and 5/6?: No.
What type of detail does visual cortex detect?: contour, shape
What do neurons in layers 2/3 and 5/6 of V1 primarily respond to?: Objects in particular ORIENTATIONS
What else besides contour and shape does visual cortex detect?: motion. Note correction/addition to earlier slide
Which fibers respond to some oriented, MOVING stimuli?: Also in 2/3 and 5/6 of V1
Are form and motion (M and P tracts) still kept separate in V1?: yes
Describe what a radial unit/column of cells in the cortex is like?: multiple single cell columns each specific for one of all possible edge orientation specificity
Where does P pathway eventually go?: From form sensors in V1 to V2 to visual cortical regionsin the TEMPORAL lope.

This is the Ventral (object recognition) pathway.
Where do nerons in the M pathway eventually go?: Motion sensitive nurons relay on to corticla regions in the PARIETAL lobe.
What is area MT?: Area of parietal cortex that are particularly sensitive to movement (in the M pathway)

If you stimulate it, it makes something stationary seem moving. If you freeze it, you lose ability to perceive motion.
Describe ocular dominance: In V1, layers outside of 4 have bilateral input. But each cell in those layers is not stimulated EQUALLY by the 2 segregated streams of info coming from layer 4. Some are, but most are dominant one way or the other. The dominance is arranged linearly...those stimulated by neurons at the border of L and R eye streams are more likely to be equally stimulated.
Explain cat suture experiment.: When they sutured one eye, then info from that eye to visusal cortex was obviously gone. Neurons in layer 4 of the cortex from the other eye (which WAS getting info) took over completely in ocular dominance, wholly driving ALL of the nurons in layers 2/3 and 5/6.
Name a possible mechanism for activtiy/experience dependent plasticity?: Ca++ regulated neurotrophin signaling
What kind of response in 2/3 cells do you see in amblyopia?: Loss of the monocular driven cells. All of the cells seem to be driven EITHER by class one or class 7 cells.
How can body supress nociceptive info?: Descending pathways can release ENDORPHINS ("opiod peptides") onto synapse area between thin fiber nociceptor and its synapse in the dorsal horn with 2d order fibers in the ST tract. This inhibits synaptic transmission
What happens upon deformation of a pacinian corpuscle?: Na AND K channels open, leading to a depolarization.
Does pacinian corpuscle have fast Na channels?: No. So a "Generator potential" is generated, analogous to a EPSP or EPP.
What is the difference in AP generation between naked nerve ending and pacinian corpuscle (which is basically a naked ending surrounded by fibroblast-like things.: Difference shows up in continuous stimulation.

Corpuscle: nerve fires only at Beginning of stim and at end.

Naked: nerve fires through duration of stimuls
what does this mean then about what corpuscle is best for?: since it fires when stim starts AND when it stops, it fires most with rapidly starting and stopping and starting stimulus--i.e., VIBRATION
Describe structure of a Merkel disk: 1) myelinated fibers branch in the skin to unmyelinated colaterals
2) Each Collateral ends in a Merkel Disk.
What happens when merkel disk compressed?: Maybe vesicles released that haave chemical with excitatory effect on the nerve terminal
Does merkel disk adapt to continued stimulus? What then is it good for?: No. Keeps firing thorughout. So it is good for sensing PRESSURE.
Why have separate receptors for vibration and pressure?: Because othherwise we wouldn't be able to tell the difference between the two. That is, if, say, Merkel disk was responsible for both, then it would likely respond pretty similarly AP-wise to continued pressure and vibration. Brain would not be able to tell the difference.
What kind of endings are the majority of nerve endings in the skin?: Not pacinian or Merkel--just free nerve endings
What size neurons are the ones that end in free nerve endings in the skin?: Usually thin unmyelinated or thinly myelinated fibers. Pain & Temp, ST style.
After injury, what order to nerves heal, and how does this manifest functionally?: 1) FIRST: thin fibers return. So you get pain, temp sensitivity and crude touch.

2) THEN: thick fibers return. So you get vibratory, kinesthesis, fine touch (graphesthesia...), 2 point discrimination
What are the two kinds of nociceptive fibers?: 1) A-delta: small myelinated
2) C fibers: unmyelinated
Describe A-delta fibers: 1) typically high-threshhold mechanorecptors or thermal receptors
2) associated with sharp, pricking pain
Describe C fibers: (small unmyelinated)

1) respond to pinch
2) but they also respond to some heat and irritant chemicals
3) associated with deep, burning pain
4) called "polymodal nociceptors"
What fibers can be "sensitized"?: C fibers.

Think getting slapped on back after sunburn. Your C fibers had been really sensitized, so you get a big burn/pinch!
What components does sensitization have?: peripheral
central
Describe peripheral component of sensitizaiton: (C fibers)

It seems that damaged skin areas locally release chemicals that sensitize areas adjeacent to the damage.
Describe central component of sensitization: Some nociceptive fibers use glutamate as their neurotransmitter in the dorsal horn.

Thus, glutamate activates AMPA, postsynaptically...if done enough, it depolarizes NMDA area enough to dislodge Mg....and LTP occurs. So you kind of primitively "learn" sensitization.
How is intenstiy of pressure conveyed by merckel disk nerve ending?: It is conveyed by the frequency of firing in the first 20 msec of stimulus
Describe the pathway of neurons that can supress nociceptive infoo?: Cerebral cortex
Periaqueductl gray (midbrain)
Reticular formation and raphe nuclei of medulla
Trigem nuclei/dorsal horn of spinal cord
Interneurons in these areas
These internurons secrete opiate-like endorphins!
Name an opiate that is as effective as morphine but doesn't depress respiratioon, doesnt lead to tolerance, and doesn't have withdrawal symptoms: ABT-594
Describe the "thermal grill" experiment: If you make a grill of alternating hot and cold bars, you activate destructive cold pain sensation, even though nociceptors not activated and neither bar temp alone would give pain sensation
What area shows increased activity in times of social rejection?: anterior cingulate
What may account for fact that pain and crude touch may return after a postcentral gyrus (s1) lesion?: There are other secondary areas (s2) dealing with those senses that may have been spared.
Describe posterior parietal syndrome: 1) leads to loss of ability to INTEGRATE sensory information from the side of body conttralteral to the lesion

2) doesn't disturb sensatoin itself

3) but it does screw up body image, spatial perception, conceptual processes
Where does posterior parietal syndrome usually occur?: Usually occurs on R brain, leading too "left neglect" syndrome
3 functions of chemosensation: 1) detection of noxious or hazardous stimuli
2) Detection of edible and nutritious food
3) Recognition of pheremones for reproduction, parental and other social behavior
Where does odor transduction occur?: In the olfactory epithelium (as compared to the respiratory epithelium of the nose)
How are olfactory receptor neurons regenerated? How often?: By action of stem cells near base of epithelium, adjacent to mature receptor cells.

Regeneration is constant and lifelong
Where in the olfactory neuron is all of the transduction machinery?: In the cilia that project out into the air.

Presenting neuron with odorants on its body draws no response
What kind of receptors are odor receptors?: 7-transmembrane segmented G-protein coupled receptor.

Similar to Opsin-type receptor found in rods and cones
Describe molecular variability of odor receptors: 400 genes
2000 odors can be detected

SO: there is not 1:1 identity between different odor and diferent receptor.
Describe molecular mechanism of odor transduction: Odor binds receptor
Receptor activates G protein
G protein activates adenylate cyclase
cAMP activates ligand-gated Na/Ca channel.
Na and Ca rush in, depolarizing cell
Is their topography in the placement of different types of olfactory receptor neurons?: Yes.
Are all ORNs tuned to just one specific odorant?: Not necessarily. Some are semi-selective for several, some seem to be more completely selective.
Where does info go from the ORNs: 1) synapses in GLOMERULUS in the olfactory bulb

2) then goes to the primary olfactory complex (uncal region) or amygdyla [via MITRAL CELLS?]
Describe interaction of different ORNs with glomerulus: It seems that only ORNs of a certain type will converge on one given glomerulus. So it is more labeled line here.
Describe the taste pathway: 1) CN 7, 9, 10 innervate tongue
2) They relay through cranial nerve nuclei
3) Taste tracts go up to VMP of thalamus
4) synapse and relay to INSULAR CORTEX (primary gustatory cortex)
Are taste cells replaced? If so, how often?: Yes.

Throughout life (like ORNs).
Relationship between sensations, receptors, and their stimuli for taste cells: Sour actually detected By cells with ion channels activated by H+

Salty detected by cells with Amiloride+ activated ion channels

Sweet: Carbos
What is common chemical sense mediated by?: Primarily free nerve endings of peripheral sensory ganglion cells, mainly of CN V
What is CCS responsible for?: Detecting irritation by airborn agents or ingested substances like menthol or capsaicin.

You need a relatively high airborne concentration to elicit a common chemical sense reation
What 2 things control/organize Motor cortex?: Basal ganglia (gate proper initiation of movement)

Cerebellum (Sensory motor coordination)
What are "lower motoneurons": Neurons in the brainstem CN nuclei and in the spinal cord that connect directly to muscle fibers
What are upper motoneurons: Neurons in the cortex (primary motor or premotor) or brainstem (vestibular nuclei, reticular formation) that connect to motoneurons
What is a motor unit?: A single motoneuron and all of the muscle fibers that it innervates
What are the 3 classes of motor units?: 1) slow
2) fast fatigable
3) fast fatigue resistant
What are S motor units composed of?: Small red muscle fibers and small motoneurons.

(lots of caps, myoglobin, and mitos)
What are FF motor units composed of?: LArger, pale muscle fibers and motoneurons
What are FFR motor units composed of?: Intermidate to FFR and FF
Where are S motor units mainly found?: Antigravity muscles (fatigue resistance helps!)
What are FF motor units good for?: Jumping, galloping
Which motor units have the most force?: FF, by far. FFR and Slow are much lower force.
Motor units and neuron size and the "size principle": Small motor units have smaller motoneurons. Large have larger.

Size principle = upon contraction, small motor units fire first, then larger.

Why? Because small neurons have high input resistance, which means a given voltage will trigger AP in it more easily (???)
Describe intra and extrafusal response system (Myotactic reflex): Intrafusal muscles have 1A afferent fibers wrapped around them. These are fast conducting.

When muscle streches, it causes 1As to fire.

1A goes back to spinal column, enters dorsal horn medially, synapses in ventral horn with motoneurons that innervate the same muscle as well as other synergistic muscles. It also synapses with interneuron that then INHIBITS motos to ANTAGOINISTIC muscles.
Where do 1As wrap around intrafusal fibers?: Around the CENTER of the fiber
How does 1A strech response stay sensitized?: By GAMMA motoneuron innervation.

These innervate contractile elements on the ENDS of the intrafusal muscle fibers.

So after strech causes 1A firing which causes contraction of the extrafusals, this creates slack in the intrafusals, so presumably 1As would STOP firing.

Instead, gamma motoneurons cause ENDS of the intrafusals to contract, taking up the slack and maintaining 1A firing--"filling in" the potential gap.
What type of motoneuron innervates the extrafusals?: alpha
Remember:: Though alpha and Gamma motoneurons can be stimulated by recurrent 1A fibers in this system, they also can be stimulated by descending tracts
What regulates muscle tone?: Input to gamma motoneurons
What happens with too much gamma excitiation/: Spasticity (hyperrefexivity, hypertonia)
What happens with too little gamma excitation: hypotonia
What are 2 major protective reflexes?: 1) Golgi tendon organ reflex
2) Flexion reflex
Where is the GTO?: Embedded in collagen fibrils of muscle tendon
What is GTO innervated by?: 1b afferents. Fast, but not as fast as 1As.
What activates 1b afferents?: TENSION. This = stretch PLUS contraction
What happens to firing rate of 1b with muscle strech alone?: No change. compare to increased firing of 1As.
What happens to 1b fibers with strech PLUS contraction of muscle?: Firing rate goes up.

For 1As, firing rate goes DOWN in this case.
What is path/effect of 1b firing?: Synapses in ventral horn with different interneurons.

INternerouns that INHIBIT the same muscle and EXCITE antagonistic muscles.
What is purpose of GTO?: Protect muscle injury in situation of vulnerability (streching, contraction)
What happens with contraction combined with excessive stretch?: 1Bs activate, causeing massive motoneuron inhibition---> cramps -->COGWHEEL rigidity
Why do you get rigidity with parkinsons?: Due to abnormal descendiing control of the GTO circuitry. so you can get cogwheel rigidity.
What happens during flexion reflex: (You step on a tack)

1) nosiceptors in dermis are activated, go back to dorsal horn.
2) some synapse and send axons across cord to go up contralateral spinothalamic tract to send pain signal to VPL.
3) some synapse with excitatory motoneurons for flexors of that leg
4) some synapse with inhib. moto. for extensors of that leg
5) some send axons to other side of cord that will excite contralateral extensors and inhibit contralateral flexoors, to keep your balance
What do you call the circuitry underlying locomotion?: CPG: central pattern generator
What are the 2 systems of descending control of lower motoneurons?: 1) from brainstem: to maintain balance and posture
2) from motor cortex: to initiate complex movements
describe the general orientataion of these 2 systems in the spinal cord:: Medial running axons tend to control posture and balance (VCST?)
What are the 2 sources of posture/balance descending control?: Vestibular nuclei
Reticular formation
Where does vestibular pathway get its info from?: inputs from inner ear for balance maintainence
Where does reticular path get input from?: brainstem, cortical motor centers.

this info helps maintain equqilibrium during ongoing movements
What does the reticulspiinal system do, generally: It ANTICIPATES postural changes and makes body ready to correct for them. e.g., when doing bicep curl, reticulospinal system causes gastroc to contract even BEFORE biceps contracts.
Where do lateral descending CST synapse?: Generally, on lateral portions of the ventral horn in the cervical and the lumbosacral enlargements. Synapse with lower motoneurons or interneurons.
Where are the original cell bodies at the start of the Coricospinal tract?: Precentral gyrus (primary motor cortex) AND premotor areas
What is relationship of CST and reticular formation?: On the way down, in pons and medulla, CST shoots off collaterals to the reticular formation, allowing for those anticipatory ccontractions in prep/response foor voluntary postural changes
Signs of damage to descending pathways: 1) babinski in adults
2) Spasticity (hyperreflexive of stretch reflexes--probably due to loss of descending inhibition), hypertonia
3) Hyperreflexive superficial reflexes (corneal, abdomninal, flexion)
4) loss of ability to perform fine movemenst (graphesthesia)
Where is the only place that the CST is isolated?: In the medullary pyramids
What happens if you make a selective lesion of the CST in the medullary pyramid?: At first, symptoms as though you lesiones whole dorsolateral funniculus (slow voluntary movements, can't fractionate movement, etc)

But eventually the only deficit remaining was ability to move fingers independently.

But if then you section RubroSpinal tract, then you get all the sypmtoms back again. So it seems that RuST is able to compensate somewhat.
Is mapping in the precentral gyrus as simple as it looks?: No. E.g., one part of the hand may be represented multiple times in distant places.
The "ensemble" stuff wrt Precentral gyrus: Supposedly, the consensus is that movement of the body (part) in one direction is encoded/initiated by an "ensemble" of neurons in the Prim motor cortex.

That is, MOVEMENTS, NOT MUSCLES are prepresennted in the precentral gyrus.
What makes up the premotor cortices?: Medial premotor cortex
lateral premotor cortex
When do neurons int he lateral premotor cortex fire?: When there is an INTENTION to make a movement
Monkey experiment with lateral premotor cortex: When the "get ready for juice" light comes on, LPMC fires.

When that goes off and the juice actually comes out, LMPC stops firing.
What does it look like to have a LPMC deficit?: They have a difficulty deciding what response to make to a visual stimulus, even though they can understand instructions and can move.
What kind of cues cause firing of LPMC: external, visual cues
When do neurons in the MEDIAL premotor area fire?: In response to internal, voluntary cue to move. This area is only active in response to internal cue to do task from MEMORY
In general, what does damage to premotor areas cause?: Apraxia---inability to develop strategies for complex movement.
What is involved in movement selection?: Medial and lateral premotor areas
FMRI and practicing hand movememtns?: If you practice a hand movement for awhile, fMRI shows that you activate more of the hand area of precentral gyrus then if you try to do a new hand motion..

But if you wait 2 months later, activation upon performing the trained sequence AND a new sequence is EVEN GREATER. (MEMORY CONSOLIDATION!)
What about supertrainig?: Professionally trained people performing motions activate a SMALLER portion of precentral gyrus than do amateurs
Which artery is the "artery of stroke"? why?: Lennticulostriate arteries. They are branches of the middle cerebral, and branch up to supply the internal capsule. One of these go, and you can take out internal capsule and cause a lot of problems.

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