L8 Flashcards

1
Q

spinocerebellar tract signals cerebellum (contra/ipsi)?

A

ipsi

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2
Q

outputs from cerebellum though to?

A

thalamus to contralateral MC.
- control of movement
info about sensory events
- info about interneurons

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3
Q

1971 hypothesis: anterior spinocerebellar tract monitors ?

A

activity of spinal interneurons

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4
Q

2001 hypothesis: posterior spinocerebellar tract neurons process inputs from?

A

inputs from muscle afferents to get limb end-point postiion

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5
Q

2016 hypothesis: limb end-point derived from ?

A

from simple summation of proprioceptive input.

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6
Q

parts of cerebellum
vermis - where? sensory control?
flocculonodular lobe AKA? Used for? mediates?
spinocerebellum - where? intermediate zone does ?
cerebrocerebellum does what?

A

v - middle, sensory control of truncal and head movement
F AKA vestibulo-cerebellum = balance and posture
S - vermis + intermediate zones.
int = sensory control of limb movements, gait
C = sensory control of complex, adaptive hand and eye movement

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7
Q

inputs to cerebellum

A

pontine nucleus
Inferiro olive
mossy fiber
climbing fiber

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8
Q

pontine nucelsi

A

from pons . input from cerebral cortex, output of mossy fibers to cerebellum

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9
Q

inferior olive

A

brainstem, neurons synapse on IO, IO project climbing fibers to cerebellum

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10
Q

mossy fiber

A

from spinal cord & brain = provide state info

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11
Q

climbing fiber

A

from IO, strongest activity during acquisition of motor sklls/novel task.effect on purkinje cells.

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12
Q

all output from cerebellum =?

A

inhibitory

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13
Q

basket cell lateral inhibition

A

inhibit purkinje cells next to it.

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14
Q

mossy fiber

A

excite purkinje cell.

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15
Q

climbing fiber

A

elicit complex spike to produce timing cues or vary sensitivity of purkinje.

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16
Q

outputs from cerebellum

A
  • purkinje via cerebellar nuclei to brain
  • inhibit nuclei to which they project.
  • alternat “side loop” if want to excite.
17
Q

cerebellum - theories of function

  1. timing, sequencing
  2. gain control
  3. balance
  4. eye movement
  5. attention, cognition
  6. motor learning
A
  1. correct msucle activation. lesion = decomposition of movement
  2. control of input-output response.
  3. lesion = body say
  4. hypertremia, involuntary oscillations of eye
  5. cerebellum active during cogntiive tasks
  6. generation of new motor programs.
18
Q

motor learnign in cerebellm studied

  • after cerebellar damage how is motor learning affected?
  • marr/albus theory
A
  • reduced/abolished motor learning.
    cerebellum maps kinematic states into motor commands.
  • learn from experience to map states into motor commands.
    parallel fiber = delay line
    climbing fiber = set gains of purkinje
19
Q

evidence for climbing fibers being teacher for purkinje

A

mediate complex spike in purknje during motor task learning, return to baseline was learnt.
causes sensitivity of parallel fiber synapses on purkinje to be modifies

20
Q

evidence for state processor role o cerebellum:

A

cerebellum areas process sensory signals to ID kinematic state in relatino to tasks and enviro are enlarged.

21
Q

BG functions

A

movement initiation

context-dependent selection of motor programs

22
Q

DeLong model of BG circuitry

A

Subs Nigra
caudate & putamen
caudate onto GP and SN (inhibitory) act on thalamus (inhibitory) act on supplementary motor.

from putamen -> inhibit GP -> inhibits STN -> excties GPi and GPe

23
Q

PD
mimicked by?
rate theory based on deLong model
treatment?

A

decreased DA.
MPTP
- GPi & SN overactive = increased inhibition in thalamus => bradykinesia.
L-DOPA, electrical lesions

24
Q

oscillatino theory of BG

A

abnormal in 10-25 hz = bradykinesia

abnormal burst at 60-80 hz = dyskinesia

25
Q

dyskinesia

  • chorea & tourrettes
  • hemiballism
A

C&T = lesion of putamen inhibit GPe - reduce inhibition of thalamus = involuntary movement
hemiballism: withdraw inhibition of thalamus = involuntary movement

26
Q

DBS
stem cells
inhibitor of dopamine breakdown

A

stem cells - clinical trials ceased.

rasagiline