Ibs 526 Exam 3

Front 1

Three main functions of cerebellum

Back 1

1. Monitor and adjust ongoing motor behavior
2. Contribute to motor learning
3. Participate in cognitive functions

Front 2

Four types of experiments to ID cerebellum function

Back 2

1. Lesions: problems solving puzzles (higher order functions)
2. Tract-tracing
3. Neural recording. Cerebellar neurons change firing frequency when limb is moved or you touch the skin.
4. fMRI, PET

Front 3

Three parts of cerebellar cortex

Back 3

Cerebrocerebellum
Spinocerebellum
Vestibulocerebellum

Front 4

Three deep cerebellar nuclei

Back 4

Dentate nuclei
Interposed nuclei
Fastigial nuclei

Front 5

Three cerebellar peduncles

Back 5

Superior
Middle
Inferior

Front 6

Define: vermis, additional name?

Back 6

Midline of cerebellum

Spino-cerebellum

Front 7

Define: Flocculus, additional name?

Back 7

bottom part of cerebellum (floppy)

Vestibulo-cerebellum

Front 8

Define: Foli, additional name?

Back 8

Folds of cerebellum

Cerebro-cerebellum

Front 9

What are the inputs to the cerebellum? (4)

Back 9

1. Cortical input (Frontal + parietal cortex -> pontine nuclei)

2. Vestibular nuclei

3. Cuneate nucleus (spinal cord, medial lemniscal pathway)

4. Inferior olive (climbing fibers)

Front 10

What are the outputs of the cerebellum? (3)

Back 10

1. (LARGE) deep nuclei project to motor + pre-motor cortex via thalamus
2. Superior colliculus
3. Vestibular nuclei

In general, everything that influences eye control, spinal cord motor control

Front 11

What is special about the vestibular cortex in the cerebellum?

Back 11

It is the only cortex (flocculus) in which fibers go out of cerebellum without passing through deep cerebellar nuclei

Front 12

Input from cerebral cortex goes to ______ in cerebellum

Back 12

Cerebrocerebellum

Front 13

Input from Pons goes to ______ in cerebellum

Back 13

Cerebrocerebellum and Spinocerebellum

Front 14

Input from vestibular organs goes to ______ in cerebellum

Back 14

Vestibulocerebellum (flocculus)

Front 15

Input from spinal cord goes to ______ in cerebellum

Back 15

Spinocerebellum, vermis

Front 16

Cerebrocerebellum outputs to _____

Back 16

dentate nucleus -> thalamus

Front 17

Spinocerebellum projects to _______

Back 17

Interposed nucleus

Front 18

Vermis projects to _____

Back 18

Fastigial nucleus -> Reticular formation

Front 19

What are the 3 layers of cerebellar cortex?

Back 19

Molecular (outer), Purkinje, Granular (inner)

Front 20

function of Purkinje cell

Back 20

Inhibitory cell in cerebellum that inhibits deep cerebellar nuclear cell

Front 21

Climbing fiber

Back 21

Excitatory cell in cerebellum that originates in inferior olive

Strongly excites multiple Purkinje cells

Serves as "teacher". Long-term depression of parallel fiber synapses

Front 22

Mossy fiber

Back 22

Originate from many different sources. Several mossy fibers synapse to a single granule cell.

Excitatory.

Front 23

Granule cell

Back 23

Neuron within cerebellum. Receives excitatory input from mossy fibers. Bifurcates into parallel fibers.

A parallel fiber can synapse only once on a specific purkinje cell

Forms WEAK excitatory synapse onto Purkinje cell

Front 24

Basket cell

Back 24

Inhibits Purkinje cell in cerebellum

Front 25

Where do the inputs to the basal ganglia come from? (3)

Back 25

1. Limbic cortex
2. Motor cortex
3. Associative cortex

Front 26

What are the outputs of the basal ganglia and what are their functions? (3)

Back 26

1. Superior colliculus: head and eye mvt
2. Thalamus: motor control
3. Pedunculo-pontine nucleus: spinal cord processing + locomotion

Front 27

Describe striatum, inputs, kinds of cells in it. Differences between primate and rodent? (5)

Back 27

1. Caudate and putamen, accumbens
2. Glutamatergic input from all areas of cortex + thalamus
3. Dopaminergic input from substantia nigra compacta
4. medium sized spiny neurons (MSNs) and striatal interneurons

In rodents, caudate and putamen are a single structure. In primates, they are separated by internal capsule

Front 28

Medium sized spiny neurons (MSNs) (3)

Back 28

90% of cells in striatum
GABAergic (inhibitory)
Main output
Slow activity at rest but active during movement/learning

Front 29

Striatal interneurons

Back 29

10% of cells in striatum
GABAergic

Front 30

What kind of terminals are highly expressed in striatum?

Back 30

Dopamine (DOPA terminals)

Front 31

What are the 3 differences between the direct and indirect pathways in the striatum?

Back 31

INDIRECT: (1) Uses enkephalins, (2) expresses D2 receptors (3) projects to GPe > STN > GPi/SNr

DIRECT: (1) uses substance P and dynorphins (2) expresses D1 receptors (3) projects to GPi/SNr directly

Front 32

External globus pallidus. Name inputs, outputs, types of each

What is it called in rodents?

Back 32

Inputs: STN (glutamatergic), striatum (GABAergic), intrinsic (local) collaterals (GABAergic)

Outputs: STN (GABAergic), GPi/SNr

Called "globus pallidus" in rodents

Front 33

What are characteristics of GPe cells? (3)

Back 33

1. Highly GABAergic
2. Glutamatergic inputs are less abundant
3. Very active (high freq. activity)

Front 34

Sub-thalamic nucleus (STN), overall, inputs, outputs (3)

Back 34

1. Mostly glutamatergic. Strongly excited by cortex. Lots of spontaneous activity.
2. Inputs: Glutamatergic: M1 and SMA; GABAergic: GPe
3. Outputs: GPe (excitatory), GPi/SNr (excitatory)
4. Reciprocal connection with GPe and STN - pacemaker activity

Front 35

Internal globus pallidus + substantia nigra reticulata (GPi/SNr)
inputs/outputs
How does it fire?
What is it called in rodents?

Back 35

Inputs: STN (glutamatergic), striatum + GPe (GABAergic)
Outputs: Thalamus, brainstem
Fires at high frequency (very active)
In rodents it is the entopeduncular nucleus (EPN)

Front 36

What is the function of GPi/SNr?

Back 36

have GABAergic projection to thalamus. Strong INHIBITION of thalamo-cortical cells.

Front 37

Substantia nigra compacta (SNc)
Inputs
Outputs
Function

Back 37

Inputs: excitatory: STN, PPN; inhibitory: striatum, SNr
Outputs: striatum (excites D1/direct, inhibits D2/indirect), STN, GPi/GPe/SNr
Function: predict reward. i.e. fire when reward occurs and after conditioning fire when they think reward will occur
If no reward occurs, their firing is depressed

Front 38

How does direct pathway of basal ganglia facilitate movement?

Back 38

Cortex excites D1 in striatum > D1 inhibits GPi/SNr > GPi/SNr weaken inhibition of thalamus > motor activity strengthened

Front 39

How does indirect pathway of basal ganglia inhibit movement?

Back 39

Cortex excites D2 in striatum > D2 inhibits GPe > GPe decreases inhibition of STN > STN excites GPi/SNr > GPi/SNr strongly inhibits thalamus > motor activity weakened

Front 40

What is the function of dopamine in the basal ganglia?

Back 40

Faciliate movement. Inhibits indirect pathway (D2) and facilitates direct pathway (D1)

Front 41

Activation of direct pathway MSNs should ______ motor activity

Back 41

Increase (activate D1 > increase inhibition of GPi/SNr > decreased inhibition of thalamus)

Front 42

Activation of indirect pathway MSNs should ______ motor activity

Back 42

Decrease (activate D2 > increase inhibition of GPe > decreased inhibition of STN > increased excitation of GPi/SNr > increased inhibition of thalamus)

Front 43

What are the possible functions of the basal ganglia? (4)

Back 43

1. Response-based inhibition (when ongoing mvt must be inhibited in response to stimulus)
2. Selecting actions from competing set
3. Control of mvt parameters (amplitude + speed)
4. Motor learning
- dopamine reinforces synapses that fascilitate behavior linked to reward

Front 44

Difference between voluntary and reflex movements (3)

Back 44

1. Not stereotyped: can use different strategies to do the same task (as opposed to knee jerk)

2. Improves with learning

3. External stimuli not necessary to evoke voluntary movement

Front 45

What 3 processes lead to voluntary movements?

Back 45

1. Target identification (posterior parietal)
2. Plan of action (premotor areas)
3. Execution of action (primary motor)

Front 46

What is Brodmann's area of primary and supplementary motor cortices?

Back 46

4 (primary), 6 (supplementary)

Front 47

What happens in the cortex after an infarct to the digit representation and subsequent rehab?

Back 47

Plasticity in the cortex. Activity dependent reorganization of motor areas. Infarct zone remains unresponsive but other representations (digit, wrist, proximal) expand

Front 48

What are the functions of the primary motor cortex? (Bueterfish) (2)

Back 48

1. Controlling distal muscles, fine digit movement
2. Functions in producing skilled movements rather than automatic/rhythmic movement.

Front 49

What properties do M1 neurons code for?

Back 49

Force. Pyramidal tract neuron (PTN) activity increases as the applied force (not displacement) increases

Also direction. Cells show preference for movement in specific directions.

Front 50

Where does primary motor cortex get its inputs from? (Bueterfish) (3)

Back 50

1. Supplementary motor area
2. Pre-motor (v and d)
3. S1

Front 51

Where do premotor areas get their inputs from? (Bueterfish) (3)

Back 51

1. S1
2. Posterior parietal cortex
3. Prefrontal cortex

Front 52

How do neurons in motor cortex get sensory feedback? (2 ways)

Back 52

1. Cortico-cortical fibers from somatosensory cortex to M1

2. Through the thalamus

Front 53

Describe function of premotor cortical areas (4)

Back 53

1. Receive input from posterior parietal cortex (ventral stream, planning action)

2. Premotor areas active before executing voluntary movement

3. Selection of tasks among alternative actions.

4. Effector (left-right arm) INDEPENDENT tuning properties

Front 54

Are premotor neurons active in precision or power tasks?

Back 54

Precision (where planning is involved)

Front 55

What is function of posterior parietal lobe? (Bueterfish) (4)

Back 55

1. Supplies information for movement towards targets
2. Information is conveyed to it from many sensors
3. Encodes kinematic information only (direction only)
4. Parietal lobe is activated more when the task is complex

Front 56

What are the three types of movements? Which ones are stereotypical and repetative? (Perreault)

Back 56

1. Reflexes: stereotypical, involuntary. Do not require descending control.

2. Rhythmic mvt (walking, breathing): stereotypical, repetitive. Require descending control

3. Directed movements: complex (writing, reaching). Not stereotypical or repetative.

Front 57

What are the three control systems of the motor system? (Perreault)

Back 57

1. Cerebral cortex (planning, control, execution)

2. Brainstem: initiation, control, execution

3. Spinal cord: integration + execution

Front 58

What are the two tuning systems of the motor system? (Perreault)

Back 58

1. Basal ganglia: selection of motor task, reward-based learning

2. Cerebellum: coordination, error-based learning

Front 59

What are the 2 types of descending pathways based on their origin?

Back 59

1. (cortex) Corticospinal and corticobulbar

2. (brainstem) Rubrospinal, tectospinal, vestibulospinal, reticulospinal

Front 60

What are the 2 descending pathways based on their terminal territory in the spinal cord? What is their function

Back 60

1. Dorsolateral: lateral corticospinal + rubrospinal (DISTAL musculature)

2. Ventromedial: medial/ventral corticospinal, tectospinal, reticulospinal (PROXIMAL musculature)

Front 61

What is the function of the corticospinal and corticobulbar pathways? Describe path (Perreault)

Back 61

Volunary control of movement

Corticospinal: M1 > cerebral peduncle > pontine fibers > pyramid > decussation (most) > (mostly) lateral corticospinal tract

Corticobulbar: M1 > cerebral peduncle > pontine fibers > cranial nerve nuclei

Front 62

What is purpose of medial and lateral vestibulospinal pathway? (Perreault)

Back 62

Balance + equilibrium

Front 63

What is the purpose of pontine + medullary reticulospinal pathway? (Perreault)

Back 63

Locomotion, reaching

Front 64

Where do nociceptors synapse in the SC?

Back 64

LI-LII (that area appears white b/c they are unmyelinated)

Front 65

Where do cutaneous mechanoreceptors synapse in SC?

Back 65

LIII-LV

Front 66

Where do Ia afferent propriocentors (muscle spindles) synapse in the SC?

Back 66

LV, LVI, LVII, LIX

Front 67

Where do Ib and II afferents (Golgi tendons) synapse in the SC?

Back 67

LV, LVI, LVII

Front 68

What is the typical organization of motor pools in SC?

Back 68

Proximal muscles > Ventral in SC

Distal muscles > Dorsal in SC

Flexors > lateral in SC

Extensors > medial in SC

Front 69

What is the difference between alpha and gamma motoneurons? (Alvarez)

Back 69

alpha motoneurons innervate extrafusal muscle fibers (Golgi tendon organs). Hevaily myelinated. Initiate contraction.

Gamma motoneurons innervate intrafusal muscle fibers (muscle spindles). Maintain spindle tone during contraction. Small, thinly myelinated.

Front 70

What are approximate innervation ratios for fine movement versus high strength movement? (Alvarez)

Back 70

Fine movement = low innervation ratio (1:10)

Strengh movement = high innervation ratio (1:2000)

Front 71

Describe motor unit recruitment (Alvarez) (2)

Back 71

1. Non-fatiguing slow muscle fibers (small motor units) get recruited first, produce little force

Fast fatiguing muscles get recruited last. Produce a lot of force but get fatigued.

2. Firing rate is modulated (up to 22 Hz b/c that is the frequency of muscle contraction)

Front 72

Why do smaller muscles get recruited first? (Alvarez)

Back 72

Big and small fiber innervated by the same neuron. Small fiber has large input resistance, so it reaches a voltage threshold easily. Large fiber has small input resistance so it takes a lot of synaptic current to reach a voltage threshold.

Front 73

Describe recruitment gain (Alvarez) (3)

Back 73

1. Sharpening of recruitment curve.
2. Bias introduced by sensory system.
3. Sensory system can excite the larer motor neuron and inhibit the smaller one.

Front 74

What is a central pattern generator (CPG)? Give 3 examples in vertabrates

Back 74

Neural network that can produce a rhythmic pattern all by itself. Does not need sensory input.

1. Locomotion
2. Respiration
3. Mastication

Front 75

Why does the absence of rhythmic activity not imply the absence of a CPG?

Back 75

The CPG can be turned off by other inputs (aka you're not always chewing)

Front 76

What are the 4 properties of CPG neurons that can lead them to oscillatory behavior?

Back 76

1. Burst firing / intrinsic oscillatory behavior: rare, cell bursts by itself

2. Bistable: plateaus triggered by short inputs. Discharge pattern outlasts input.

3. Post-inhibitory rebound: neuron fires as it recovers from hyperpolarization

4. Spike-frequency adaptation: decrease in firing frequency during constant depolarization (slowly adapting response)

Front 77

What are the 2 factors that contribue to making CPGs rhythmic?

Back 77

1. Intrinsic properties of neurons that make up the network: neurons can act as core oscillator, causing the rest of the circuit to oscillate

2. Properties of synapse (strength, time): synaptic interaction makes the oscillation. Typically reciprocal inhibition

Front 78

Describe reciprocal inhibition (Hochman CPGs)

Back 78

Two neurons that fire non-rhythmically in isolation fire in alternating bursts when they inhibit each other. Part of synapse-based rhythms.

Front 79

Describe circuitry of CPG network responsible for swimming

Back 79

Left and right compartments receive inputs from reticulospinal tract

Each compartment has excitatory interneurons (EIN), inhibitory interneurons (IIN), commisural interneurons (CIN), and motoneurons (MN).

1. EIN on one side gets excited > excites CIN, IIN, MN
2a. CIN inhibits opposite compartment
2b. IIN inhibits EIN and MN
2c. MN fires
3. CIN is inhibited by the inhibition of EIN, so other side becomes less inhibited

Front 80

Why do two different neuronal populations cover the range of swimming techniques?

Back 80

High freq. range = fight or flight response

Low freq. range = normal locomotion

Front 81

What does the frog metamorphosis process say about CPGs?

Back 81

When both tail and legs are present:

5-HT and NA can synchronize/couple the tail CPG to the leg CPG. Without neuromodulation, they are doing their own thing and swimming is impaired.

Front 82

In cat locomotion, ________ are active during the swing phase and _______ are active during the stance phase of motion

Back 82

flexors, extensors (although there is some overlap)

Front 83

What is a piece of evidence for the existance of half-centers in the spinal cord?

Back 83

When L-Dopa is administered to spinal cord and e-stim to flexor reflex afferents in spinalized cats, the muslces produced a walking motion. (no other sensory inputs).

This shows reciprocal inhibition between ipsi- and contralateral half-centers

Front 84

What is the unit burst generator hypothesis? (CPG)

Back 84

CPG circuits can be coupled together to produce complex motions. I.e. the circuits can burst on their own but depending on what motion you want to do, additional circuits can be recruited.

Front 85

What are the two hypotheses of patterned limb movement generation?

Back 85

1. Half-center
2. Unit burst generator

Front 86

What are the 4 features of locomotion? (Hochman, CPG)

Back 86

1. Supraspinal structures are not necessary for basic motor pattern generation

2. Rhythm produced by circuits IN the spinal cord

3. Circuits are activated by non-oscillating input from the brain

4. CPG networks do not require sensory inputs but are modulated by them

Front 87

What molecules have been shown to generate locomotion when applied to the spinal cord?

Back 87

5-HT, NMDA, DA

Front 88

What are 2 types of motor system controls?

Back 88

1. Feedforward (CPGs, rhythm generation)
2. Feedback

Front 89

What are the coordinate transformation in the bladder system?

Back 89

None. Detrusor muscle has stretch receptors

Front 90

What are the two control systems of the bladder?

Back 90

1. Micturition reflex
2. Feedforward suppression of micturition reflex

Front 91

What coordinate transformations is involved in control of eye movements?

Back 91

1. Muscle length and force to eyeball rotation

Front 92

What feedback control is involved in control of eye movements? (4)
Does it require coordinate transform?

Back 92

1. Smooth pursuit of moving targets
2. Accomodation - pupils adjusting to focus
3. Vergence (both eyes moving towards or away from e/o)
4. Pupillary dilation in response to light

No coordinate transform.

Front 93

What feedforward control is involved in control of eye movements (2)
Does it require coordinate transform?

Back 93

1. Voluntary saccade
2. Vestibulo-ocular reflex (using vestibular organs to control eyes)

Requires coordinate transformation

Front 94

What is Listing's law?

Back 94

The eye exhibits torsion. going from one one position of eye to another requires rotating about an axis that lies in the plane orthogonal to the gaze of the first eye position.

Front 95

What are the two DOFs in the eye?

Back 95

1. Torsion
2. Rotation.

Front 96

What coordinate transforms are required in skeletomotor control? (3)

Back 96

1. Muscle length/force to joint rotation
2. Joint rotation to trunk/head movements
3. VIsion to limb movement

Front 97

What coordinate transform are parkinsonian patients unable to make?

Back 97

Vision to limb movement. Errors in memory reaching tasks.

Front 98

What is active lengthening in skeletomotor control?

Back 98

The TA muscle tries to contract when you step down. So it is being expanded but is trying to contract. (going down the mountain). Loading determines muscle activity.

Front 99

What is goal equivalent variance? What is its purpose?

Back 99

Two different configurations of limbs produce the same outcome (Bernstein's factory workers).

Purpose is to prevent little things from screwing up the movement.

Front 100

What coordinate transforms need to occur in skeletomotor systems?

Back 100

1. Vision to limb movement
2. Proprioception to limb movement.

Front 101

What are hierarchical control systems for skeletomotor systems? (4)

Back 101

1. Intrinsic mechanical properties of muscle
2. Local feedback
3. Equilibrium points
4. Internal models

Front 102

What happens to patients with no proprioceptive feedback during reaching tasks?

Back 102

Odd trajectories during targeted reaching. They cannot control the inertial properties of limbs.

Front 103

What are 3 elements of postural equilibrium? (staying in balance) (Ting)

Back 103

1. Feedforward (anticipatory) control of balance
2. Feedback (reactive) control of balance
3. Choosing from multiple solutions

Front 104

Describe postural equilibrium (ting)

Back 104

Standing balance is a dynamic task. Center of pressure and center of mass keep shifting.

Front 105

Describe feedforward balance control (Ting)

Back 105

Standing lever example. Ankle muscles get activated before the lever is pulled to keep the body in equilibrium (unless the body is otherwise stabilized).

Front 106

Describe reactive (feedback) balance control (Ting)

Back 106

Task level (move COM) > Execution (Activate muscles) > Execution (Muscles stretched, foot pressure uneven) > Task (COM is tilted to right/left) > start over.

Sensory receptors + muscles important

Front 107

Explain the integration of sensory information for postural equilibrium (Ting). Role of 3 senses?

Back 107

NEED MULTIPLE SENSES.

Somatosensory receptors necessary for timing.
Vestibular + visual modulate

Flexible reliance on senses

Front 108

Describe how stretch reflex is not enough to maintain posture (ting)

Back 108

<<Guy on rotating platorm slide>>
If platform is flat and translates back, calf gets activated (due to STRETCH response), which is fine.
If platform rotates upwards, stretch response (spinal mediated) activates calves initially but that is bad so postural response (brainstem) corrects it by activating TA.
If platform rotates down, TA gets activated as a stretch response but calf gets activated later as a postural response.

Front 109

Example of how visual and vestibular info alone is insufficient to maintain posture (ting)

Back 109

Visual: if picture is spinning, you start leaning in the direction of rotation
Vestibular: if we turn, vestibular system picks it up and defines a new "vertical"

Front 110

Describe how vestibular info is bad (ting)

Back 110

<< person with eyes closed on a platform slide>>
Small perturbation in platform tilt > muscle spindles > tilt with platform
Large perturbation > vestibular takes over > orient with gravity (unless they have vestibular lesion)

Front 111

Examples of how a single sense is insufficient for maintaining postural equilibrium (ting) (4)

Back 111

1. Stretch reflexes (tilting platform)
2.Vestibular (tilting platform)
3. Vestibular otoliths (can't tell linear accel vs head tilt)
4. Visual (cannot tell self-motion from object motion)

Front 112

What is special about postural perturbation? (ting)

Back 112

common goal (maintaining balance), different execution strageties (leg move, hip move etc)

Front 113

What is the timetable of postural responses to perturbation? (ting) (4)

Back 113

0. Perturbation
1. Passive response + sensory feedback
2. Spinal response (monosynaptic stretch reflex, only in stretched muscles) (50 ms)
3. Brainstem response activates different muscles depending on situation (100 ms)
4. Voluntary response, cortex, (> 250 ms)

Front 114

Describe ankle strategy vs hip strategy. Describe experiment (ting)

Back 114

Ankle strategy: using back, leg, calf muscles to maintain equilibirum
Hip strategy: Swinging hips to maintain posture (like when you are on a beam that slides back).

Experiment shows that after doing many trials on the beam you habituate and automatically do the hip response even when you're back on the floor. After several trials, you're back to ankle strategy

Front 115

Describe response of parkinson's patients to perturbation (ting)

Back 115

Basal ganglia deficit -> cannot select appropriate muscles to activate based on context (leg muscles active when seated)

Front 116

Describe response of cerebellar patients to perturbation (ting)

Back 116

Over-respond to perturbations, oscillate. Do not adapt to blocks of the same perturbations. b/c they cannot use prior info to modulate response

Front 117

What cues give you a hint about initial hand position with respect to target (Sober I)

Back 117

Visual and proprioceptive

Front 118

What computations are important for reach planning (5)? (Sober I)

Back 118

Retinal position of target > position of target in space > eye to head > head to torso > torso to object >>> motor command

Front 119

What coordinate transformations underlie reaching? (Sober I)

Back 119

Visual coordinates > joint angle coordinates > hand position

Front 120

Describe motor babbling (Sober I)

Back 120

Babies wave seen hand more and resist a weight to SEE their hand move. Observe sensory consequences of movement

Front 121

Define reafference, example (Sober I)

Back 121

Sensory stimulation from self-produced movements
Crucial in development. Kitten in box does not develop important abilities (cliff avoiding, blinking at approaching object) b/c it does not observe the consequences of its own actions even though it gets the same visual input as the active kitten.

Front 122

Describe basic prism google experiment (Sober I)

Back 122

Ask person to reach for target. Put on prism goggles (shift view left/right), ask to reach again. Take off, ask to reach again. Big errors in reach as soon as you put goggles on and as soon as you take them off (after-effect). AFTER-EFFECT indicates there was a re-mapping in the brain due to the goggles.

Front 123

How to separate sensory (arm-independent) from motor (arm-specific) effects in prism goggle experiment? AKA where is the remapping being done? (Sober I)

Back 123

Transfer task to the other hand. If MOTOR aspect is being remapped in the brain, there will not be transfer (no after-effect). If SENSORY aspect is being remapped in the brain, there will be transfer (after-effect) with the opposite arm.

Front 124

Second method of separating sensory from motor effects in prism goggle experiment? (Sober I)

Back 124

Perception of “straight ahead” (Not clear)

Front 125

How can you figure out whether active of passive exposure matters in the prism goggle experiment (Sober I)

Back 125

Have experimenter move the arm for the person to the target.
Person does not learn > no after-effect

Front 126

What are 3 classification schemes for movement disorders? (Wich)

Back 126

Hyperkinetic vs hypokinetic
Primary vs secondary
Focal vs generatlized (single muscle vs all muscles)

Front 127

What are the 2 models of motor dysfunction In basal ganglia? (Wich)

Back 127

Rate models: amount of mvt is determined by the firing RATES of neurons in basal ganglia, thalamus, cortex
Oscillation models: BG – thamaus circuits exhibit oscillatory activity

Front 128

What are 4 characteristics of parkinson’s disease (parkinsonism)? (Wich)

Back 128

Tremor at rest
Akinesia (freezing in front of edges, decreased arm swing etc) HYPOKINETIC
Bradykinesia
Rigidity

Front 129

What is the biochemical principle of parkinson’s disease? What is it / is it not correlated with (Wich)

Back 129

Dopamine depletion in the striatum
Loss of dopamine is correlated with parkinsonism (tremor, akinesia, rigidity) but not with other issues (dementia, balance problems etc)

Front 130

Describe rate model for Parkinson’s

Back 130

SNc no longer acts on striatum (excite D1, inhibit D2)
Indirect pathway increased, direct pathway inhibited
GPe inhibited > STN excited > GPi/SNr excited > Thalamus inhibited > cortex inhibited > mvt inhibited

Front 131

Describe Oscillatory model of parkinson’s (Wich)

Back 131

In normal patient, beta band is desynchronized before movement and synchronized after movement; gamma band is synchronized before movement and desynchronized after movement
In Parkinson patients, this is flipped.
This may result in akinesia (freezing, decreased arm swing)

Front 132

Is chorea hypokinetic or hyperkinetic (Wich)

Back 132

HYPERkinetic (ongoing, flowing movements)

Front 133

Is parkinsonism hypokinetic or hyperkinetic (Wich)

Back 133

HYPOkinetic (slowing down)

Front 134

Describe action of D2R-agonist induced chorea (Wich)

Back 134

Indirect pathway decreased.
GPe firing increases > inhibits STN (disinhibits GPi/SNr)
Excitation of GPi/SNr by STN decreases > less inhibition of thalamus > more thalamic output to cortex > more movement
Direct pathway is also more active (same effect)

Front 135

Describe picture of hemiballismus (Wich)

Back 135

Stroke of sub-thalamic nucleus (STN)
Indirect pathway no longer active
Direct pathway inhibits GPi/SNr > GPi/SNr don’t inhibit thalamus as much > thalamus activity increased > cortex activity increased > movements increased

Front 136

Describe pathology of Huntington’s disease (Wich)

Back 136

Loss of indirect pathway neurons in striatum (genetic)

Front 137

Describe clinical manifestation of Huntington’s (Wich)

Back 137

First, chora (hyperkinetic), then parkinsonism (hypokinetic)

Front 138

Describe picture of Huntington’s

Back 138

Indirect pathway deteriorates
GPe strongly inhibits STN (and GPi/SNr) > STN no longer excites GPi/SNr
Thalamus no longer inhibited by GPi/SNr > more movement

Front 139

What is the current prominent treatment of Huntington-induced chorea

Back 139

Make patient slightly parkinsonian (Dopa receptor blockers) to stop movements, induce hypokinesia

Front 140

What are clinical features of dystonia?

Back 140

Slow, sustained involuntary muscle contractions, abnormal poses (writer’s cramp)

Front 141

What is the pathophys. of dystonia? (3) (Wich)

Back 141

Low levels of cortical inhibition
Abnormal mapping in sensory/motor cortices
Dopaminergic dysfunction

Front 142

What is the flow of information in the cortical areas during motor function? (Sober II)

Back 142

Visual > parietal > frontal > premotor > motor>muscles

Front 143

What is the function of posterior parietal cortex and how was it determined? (Sober II)

Back 143

Function: preparation to reach.
How: Present cue to monkey (where it should reach to get reward) > turn cue off > present GO auditory cue to monkey
Poterior parietal neurons active between 1st cue and GO cue -> NOT visual neuron

Front 144

What is intrinsic vs extrinsic (Sober II)

Back 144

Intrinsic – more muscle-like
Extrinsic – position + direction

Front 145

What experiment helped ID whether PPC / M1 were extrinsic / intrinsic? (Sober II)

Back 145

Assistive reaching tasks
Neurons in M1 were correlated to EMG signals (more load > more EMG > more M1 activity) – ENCODES FORCE
Neurons in PPC were direction-oriented (load had no impact on firing rate if the monkey was reaching to the same target – ENCODES LOCATION

Front 146

(Strick paper) How can you tell if a neuron is EXTRINSIC from its firing pattern in the 3 hand on lever positions? (Sober II)

Back 146

If neurons’s activity is the same in all 3 types of grabs, it is extrinsic (responds to DIRECTION of motion, not specific hand orientation). I.E. it responds to the “left” orientation in ALL grab types

Front 147

(Strick paper) How can you tell if a neuron is INTRINSIC from its firing pattern in the 3 hand on lever positions? (Sober II)

Back 147

Look across all grab types. If the neuron’s firing rate changes from grab type to grab type, it is intrinsic. I.E. Neuron is sensitive to “Up” in the pronated posture but sensitive to “Down” in the supinated posture.

Front 148

What kind of coordinate frames are in the (1) PMv, (2) M1, and (3) muscles? (Sober II)

Back 148

PMv: all extrinsic; M1: some intrinsic, some extrinsic; muscles: all intrinsic

Front 149

What is the evidence that the cerebellum is involved in motor learning

Back 149

Throwing stuff at targets with/without prism goggles experiment
In normal brain, put on prisms > throw location is initially off > take off prisms > throw location is initially off (after-effect)
In patient w/ lesion, NO improvement in throw location with prisms on, NO after-effect -> no learning

Front 150

Describe the single-neuron motor learning experiment (Sober II)

Back 150

Monkey w/ joystick (in a force field), with cursor, performing reaching tasks
No force-field -> reaching is straight
CCW force field -> reaching curves bend CCW EARLY, go back to straight after training
Early washout (NO force field) -> after-effect (trajectories curve CW initially)

Front 151

What would the tuning curves for a kinematic neuron look like in the force field experiment (Sober II)

Back 151

Kinematic = extrinsic
No change in tuning between baseline, force field, and washout

Front 152

What would the tuning curves for a dynamic neuron look like in the force field experiment (Sober II)

Back 152

Dynamic = intrinsic
Oriented one way for baseline and washout, a different way for force field

Front 153

What would the tuning curves for a memory neuron look like in the force field experiment (Sober II)

Back 153

Tuning changes from baseline to force field, but stays that way after washout

Front 154

What is the function of the posterior parietal cortex? (Sober II)

Back 154

Align proprioception of arm with vision of hand
Compute hand position in space
Compute target position in space

Front 155

What is the function of the premotor cortex? (Sober II)

Back 155

Code the desired movement by “subtracting target position from hand position”

Front 156

What is the function of the M1? (Sober II)

Back 156

What is the function of the M1? (Sober II)

Front 157

Define motor pool (Alvarez)

Back 157

All motoneurons innervating a single muscle

Front 158

What are 4 strategies to view spinal cord connectivity? (Perreault)

Back 158

1. Transynaptic viral tracers
2. Calcium recording
3. Photostimulation
4. Optogenetics

Front 159

What will a bilateral lesion to the pyramids do to a monkey doing intricate hand work? (Perreault)

Back 159

Lesion affects lateral corticospinal tract so monkey will not be able to do voluntary control of fine movement.