Hef - Cerebellum, basal ganglia, cortical function Flashcards

1
Q

cerebellum functions

A
  • sequence of motor activities and corrects movements (corrective action)
  • predictive action
  • compare efferent motor from cerebral cortex and spinal cord info. to afferent proprioceptor info.
  • planning movements - learns from mistakes
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2
Q

what does cerebellum receive inputs from?

A
  • efferent copy neurons from motor cortex or interneurons in spinal cord
  • reafferent info. from muscle spindles, Golgi tendons, and proprioceptors
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3
Q

Purkinje fibers

A
  • ALWAYS inhibitory to DCN by releasing GABA
  • stops the signal or prevents overshooting or oscillation
  • ataxia with DCN lesion
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4
Q

climbing fibers

A
  • supply low # of Purkinje fibers
  • communicate with DCN and higher centers
  • direct action Purkinje cells, DCN, and accessory cells
  • COMPLEX spikes
  • comparing and building memory - TEACHERS
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5
Q

mossy fibers

A
  • supply high # of Purkinje cells
  • communicate with granule cells –> signal to Purkinje cells
  • SINGLE spikes
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6
Q

other inhibitory cells of cerebellum

A
  1. basket, stellate, Golgi
    - can participate in lateral inhibition –> sharpen signal
    - always inhibitory
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7
Q

vestibulocerebellum

A

predictive calculations to make anticipatory corrections to prevent one from losing balance

  • direct projections to vestibular nuclei to provide sense of movements
  • able to override the VOR when necessary
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8
Q

spinocerebellum

A

receive info. from spinal cord - feedback control of distal limb movements
-receive copy efferent and reafferent info. then signal to DCN –> cerebral cortex and red nucleus

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9
Q

cerebellum dampening functions

A
  • prevent overshooting –> ataxia leads to loss of coordination, hypotonicity, and jerky movement
  • prevent back and forth oscillation –> lesion lead to end tremors
  • facilitate rapid alternating movements –> lesion lead to dysdiadochokinesia
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10
Q

cerebrocerebellum

A
  • communicate with primary, supplementary, and premotor cortex
  • damage lateral zones –> lose coordination
  • planning and timing of sequential movements
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11
Q

Purkinje fiber affecting movement

A

fire Purkinje –> release GABA –> inhibit DCN –> inhibit motor neuron
-fire motor neuron when Purkinje stops signaling

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12
Q

static vs. dynamic balance

A

static = balance and posture when not moving

dynamic = balance and posture with extreme movement

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13
Q

function of the basal ganglia

A
  • select important moves
  • operational learning
  • default –> suppress all movements (damage leads to rigidity and tremors)
  • multitasking –> chunking (piece together info.)
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14
Q

basal ganglia inputs

A
  • input from cerebral cortex to striatum releasing GABA
  • substantia nigra –> dopamine
  • thalamus –> glutamate to signal cerebral cortex
  • STN –> nucleus
  • raphe nucleus –> serotonin
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15
Q

output/intercommunication

A
  • medium spiny neurons –> GABA

- interneurons –> ACh (inhibited in parkinsons)

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16
Q

basal ganglia outputs

A

SNr and GPi –> always inhibitory

-signal to thalamus, pontomedullary reticular formation, and superior colliculus

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17
Q

role of dopamine

A

found in substantia nigra (compact) –> Parkinson’s with damage

  • tonic release –> steady state
  • phasic release –> exaggerate signal –> punding
  • amphetamine, cocaines, and antagonists increase dopamine levels –> movement
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18
Q

hyperdirect pathway

A

use myelinated axons –> stop all actions (INHIBITORY)

  • fastest response
  • cerebral cortex sends a copy signal to subthalamic nucleus –> + GPi –> release GABA inhibiting thalamus –> no feedback to cortex –> shut down muscles
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19
Q

direct pathway

A
  • lose complex functions in parkinsons
  • stimulatory and initiates movement
  • dopamine acts on D1 –> tonic
  • stimulate striatum –> inhibit GPi with GABA –> less GABA released from GPi –> less inhibition on thalamus –> stimulate cerebral cortex
20
Q

indirect pathway

A

net effect is inhibitory

  • lesion –> excess movement
  • striatum release GABA to GPe –> less GABA release to STN and GPi –> + GPi –> inhibit thalamus –> no response
21
Q

Parkinson’s disease

A

degeneration of dopamine neurons in SNc

-loss of DIRECT pathway –> no movement

22
Q

hemiballismus

A

contralateral STN lesion –> lose inhibition on thalamus bc GPi is not stimulated as much –> unusual arm movement

23
Q

Huntington disease

A

degeneration of striatum –> unusual movement

24
Q

rigidity

A

increased resistance to passive limb movement

  • lead pipe –> BG lesion –> continuous rigidity throughout stretch
  • cogwheel –> rigidity with phases
25
Q

dystonia

A

abnormal position of limbs, face, trunk

-result from antipsychotic drugs –> hypersensitivity when taking dopamine antagonists

26
Q

athetosis

A

twisting movement of limbs, face, trunk

  • chorea
  • same treatment as parkinson’s
27
Q

chorea

A

continuous, involuntary movement that gets jerky when getting worse

  • see in Huntingtons
  • loss of INDIRECT pathway –> lose inhibition
28
Q

hemiballismus

A

excess movement of proximal limb muscles - unilateral movement

  • cause by infarct in STN
  • problem with indirect pathway
29
Q

tremors

A

rhythmic oscillating movements

-resting, postural, or intention (ataxic)

30
Q

idiopathic parkinson’s disease

A

loss of dopamine in SNc (loss of pigmented neurons)

  • deficiency of dopamine for direct path –> D1 receptors and tonic –> lead to rigidity and hypertonia
  • deficiency of dopamine for indirect path –> D2 receptors and phasic –> lead to tremors
31
Q

L-dopa

A

precursor for dopamine –> treat parkinson’s

  • on/off response
  • some basal ganglia cells are cholinergic fibers –> alternate b/w ACh and dopamine when treating to prevent tolerance
32
Q

Huntington’s disease

A

excess movement at 1st but muscle waisting over time –> lose movement all together

  • progressive atrophy of striatum
  • no treatment
33
Q

parieto-occipito-temporal association area

A
  1. wernicke
    - language and cognition on dominant side
    - humor and metaphors on non-dominant side
  2. angular gyrus
    - metaphors, memory retrieval
    - damage –> word blindness (understand something said to you but not shown to you)
34
Q

prefrontal association area

A

associated with thoughts, working memory, verbal, planning, limbic system, intelligence, face recognition
-lobotomy –> loss of complex problems, planning, social problems, train of thought, mood changes

35
Q

broca vs. wernicke area

A
  1. broca
    - motor speech on dominant
    - variable tones on non-dominant
  2. wernicke
    - language on dominant
    - humor, metaphors on non-dominant
36
Q

aphasia

A

language deficit from lesions in same hemisphere

  1. broca (nonfluent) - can understand, unable to speak
  2. wernicke (fluent) - cannot comprehend or differentiate words, speech normal
  3. conduction - cannot repeat word, but can say word if shown
37
Q

corpus callosum

A

connect right and left hemispheres for bilateral functioning - crosses fibers for collaboration/coordination

38
Q

working/immediate memory

A

holds info. relevant to current task - hold onto thoughts for a few sec.

  • necessary for reading
  • can’t remember info.
39
Q

2 types of memory loss

A
  1. anterograde amnesia - cannot store new info.

2. retrograde amnesia - cannot retrieve memory

40
Q

short term memory

A
  • lasts for seconds or hours
  • reverberating circuits
  • faciliation causes memory to last longer
  • tetanic stimulation: Ca2+ accumulation - more likely to fire
  • posttetanic potentiation: Ca2+ level maintained
41
Q

habituation - short term memory

A

loss of response due to Ca2+ not opening as well from repeated stimulation –> less Ca2+ influx –> less NT –> lose response

42
Q

facilitation - short term memory

A

noxious stimulus gives you serotonin –> increase cAMP –> keeps Ca2+ open longer and closes K+ channels –> depolarize longer –> more NT release –> exaggerated response with any stimulus after that
-go back to normal when serotonin is gone

43
Q

long term memory

A
  • declarative - facts
  • procedural - motor skill retention
  • remodeling of synapses of receptors –> long lasting memory
44
Q

long term memory mechanism - potentiation

A

glutamate binds to AMPA and NMDA receptors

  • excess glutamate –> + AMPA –> Na+ displaces Mg2+ from NMDA exchanging for Ca2+ –> increase expression of AMPA and NMDA –> exaggerate response
  • Ca2+ entry provides NO release –> more glutamate release from presynaptic neuron
  • increase # of receptors and synapses
  • EtOH is inhibitor of NMDA –> lose memory
45
Q

hippocampus

A

memory forming center

  • organizes info into long term memory
  • help coordinate and consolidate memory in cerebral cortex
46
Q

Alzheimer’s disease

A

atrophy of the brain

  • deficiency of ACh and nerve growth factor
  • treatment –> prevent B-amyloid production, give NGF, or stop ACh breakdown