Motor Systems 3 - Ebner Flashcards

1
Q

Cerebellum is organized contralaterally, bilaterally, or ipsilaterally?

A

Ipsilaterally

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2
Q

What cells are the origins of the parallel fiber network?

A

Granule cells

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3
Q

What are the three inhibitory interneurons of the cerebellar cortex?
What NT do they use?
What are they activated by?

A

Stellate, basket, and Golgi cells
All use GABA
All excited by parallel fibers

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4
Q

Are granule cells excitatory or inhibitory?

What NT do they use?

A

Excitatory

They use glutamate

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5
Q

What do purkinje cells receive afferent input from?

A

They receive EXCITATORY input from parallel fibers and climbing fibers

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6
Q

What do purkinje cells output to?

A

They are inhibitory to cerebellar nuclei/vestibular nucleus

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7
Q

Describe the differences in input between mossy fibers and climbing fibers and their effects on purkinje cells:

A

a. Mossy fiber afferents:
- Originate in spine and brainstem
- Synapse on granule cells (excitatory, glutamate)
- Produce “simple spikes” in Purkinje cells
- High frequency discharge
- Encode temporal and intensity information

b. Climbing fiber afferents:
- Originate in inferior olive ONLY
- Monosynaptic to Purkinje cells
- Powerful excitation
- Produce “complex spikes” in Purkinje cells
- Low frequency discharge
- May encode “teaching signal”

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8
Q

What is the vestibulocerebellum in charge of?

A

Vestibular, balance, and eye movements

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9
Q

What kind of input does the vestibulocerebellum get?

A

MOSSY FIBERS carry info from:
Semicircular canals
Otoliths
Visual info from parietal and occipital to pontine nuclei

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10
Q

Where does the vestibuloverebellum send its outputs?

A

Projects to vestibular and fastigial nuclei (medial and lateral)

Medial vestibulospinal tract
(controls trunk/neck muscles)

Lateral vestibulospinal tract
(controls limb muscles)

Gaze centers
(controls eye movements)

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11
Q

If the vestibulocerebellum is damaged what kinds of signs do you get?

A
  • Disturbances of equilibrium/balance – fall toward side of lesion
  • Nystagmus
  • Loss of smooth pursuit eye movements
  • (Lesioning the fastigial nucleus has similar effects)
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12
Q

What is the spinocerebellum in charge of?

A

Monitor and coordinate ongoing movements, especially in lower limbs

(This wasn’t from lecture, but I think it’s right)

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13
Q

What kind of problems will you get if you injure the spinocerebellum?

A

Gait ataxia
Hypotonia (this is odd because its a central lesion)
Voluntary tremor (shake when you move)
Limb ataxia/dysmetria
Problems with timing (disdiadochokinesia)

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14
Q

Where does the cerebrocerebellum git its inputs from?

A

Pontine nuclei,

from sensory, motor, premotor, and parietal cortices

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15
Q

Where do the outputs of the cerebrocerebellum go?

A

Via dentate nuclei:

Ventral nucleus of thalamus to motor/premotor in order to control corticospinal tract
PRefrontal area
red nucleus to rubrospinal tract

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16
Q

What kind of problems do you get with a lesion of the cerebrocerebellum?

A

Ataxia of the fienst movements
-shaping of hands, writing
(Same effects when dentate nucleus is damaged

17
Q

Where does the climbing fiber system arise from? How is it organized in comparison to the purkinje cells?

A

It arises from the contralateral inferior olive

It projects parasagitally to Purkinje fibers orthogonal (perpendicular) to parallel fibers

18
Q

So overall, cerebellum’s main job?

A

Produce smooth and coordinated movements
Help movement timing
Create motor learning
Predict and improve consequences of motor movement

19
Q

How do Purkinje cells influence motor learning?

A

Through long term depression of parallel fibers at the purkinje cell synapse
Conjunction of climbing fiber and parallel fibers to Purkinje cells

20
Q

How does Long term depression occur in the cerebellum?

A

Basically parallel fibers and climbing fibers have to be activated simultaneously on Purkinje cells. The Ca influx created by the climbing fibers works to actually decrease the response of AMPA receptors to glutamate at parallel fiber synapses

So LTD selectively reduces transmission at the parallel synapse.

21
Q

What happens in mice who have Purkinje cell specific loss of LTD?

(specifically when to their VOR plasticity?)

A

The lose their VOR plasticity

Their brain is unable to mold the new sort of input that they are getting from magnified lenses and they are never able to learn it.