Week 4 - The Cerebellum Flashcards

1
Q

why does the cerebellum have more neurons than the rest of the nervous system combined?

A

all the granule cells in the granule layer

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2
Q

what are the 3 functional cerebellar zones, their cortex regions, and human/mammalian deep nuclei nomenclature?

A

midline - in vermis; fastigial/fastigius or medialis, and vestibular/vestibularis
intermediate - in paravermal hemisphere; globose/interpositus anterior and emboliform/interpositus posterior
lateral - in lateral hemisphere; dendate/dentatus or lateralis

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3
Q

what are the putative motor and cognitive functions for the midline cerebellar zone?

A

motor: balance, eye movement, reflexes
cognitive: autonomic arousal, limbic regulation

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4
Q

what are the putative motor and cognitive functions for the intermediate cerebellar zone?

A

motor: sensorimotor integration, movement execution
cognitive: simple verbal responses to commands

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5
Q

what are the putative motor and cognitive functions for the lateral cerebellar zone?

A

motor: preparation and planning of movements, fine motor dexterity, eye movements, imagined movements
cognitive: verbal association, rule-based learning, working memory, problem-solving, monitoring performance, temporal perception

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6
Q

what are the 3 cerebellar zones that can be defined based on the source of strongest inputs?

A

spinocerebellum/paleocerebellum - medial (includes vermis)
vestibulocerebellum/archicerebellum - inferior (nodulus and flocculus)
cerebrocerebellum/neocerebellum - lateral

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7
Q

what are the 3 basic elements of the cerebellum? what are their components?

A
  • cerebellar cortex (granule, Purkinje, and molecular layers)
  • deep cerebellar nuclei (output structures)
  • large white matter tracts (connect cerebellum with other structures)
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8
Q

what are the 6 main types of neurons in the cerebellar cortex?

A

granule, Golgi, Purkinje, stellate, basket, and Lugaro

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9
Q

what are the neurons in deep cerebellar nuclei?

A

only two: projection neurons and local interneurons

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10
Q

what are non-neuronal cells in cerebellum?

A
  • radial/Bergmann glial cells (in Purkinje and molecular layers of cortex)
  • bushy astroglia (in granule layer)
  • oligodendrocytes (in white matter)
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11
Q

what are the cells in the 3 cerebellar layers?

A

granule (inner): granule cells, mossy fibers, Golgi cells, climbing fibers, and Purkinje cell axons
Purkinje (middle): Purkinje cell, Golgi fibers
molecular (outer): Stellate cells, basket cells, parallel fibers, Purkinje dendrites

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12
Q

where do climbing fibers come from and where do they go?

A

come from inferior olive, and twirl around Purkinje cells

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13
Q

what are the 3 basic types of evidence used to determine types of functions that the cerebellum is involved in?

A
  1. anatomical data to define what areas of the brain participate in cerebellar circuits, and thus what types of signals the cerebellum is likely to process
  2. physiological data from imaging studies and recordings of cerebellar cells have indicated which cerebellar regions and neurons are active during specific types of tasks
  3. data from clinical, pathological, and behavioral studies have revealed what the functional consequences of cerebellar damage are
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14
Q

what is the main output cell of the cerebellar cortex?

A

Purkinje cell
-inhibit deep nuclei that powerfully facilitate thalamus and motor cortex or other brainstem motor nuclei to facilitate movement

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15
Q

what kind of action potentials do Purkine cells fire?

A

simple spikes and complex spikes

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16
Q

what are simple spikes?

A

typical neuronal APs produced by mossy fiber activation of granule cells, leading to parallel fiber activation of Purkinje cells

  • neuron’s membrane voltage changes from -50 mV to +50 mV, then returns to resting membrane potential in less than 3 ms whenever sum of inputs from other parallel fibers exceeds threshold voltage
  • occur in predictable fashion w/ variety of volitional movements (arm, head/neck, eye movements)
  • related to specific aspects of movement (moment to moment changes in behavior)
17
Q

what is “efference copy” or “reafference”?

A

moment to moment changes in behavior, related to simple spikes of Purkinje cells

18
Q

what are the 4 major precerebellar spino/medulo cerebellar tracts?

A
  • dorsal spinocerebellar
  • ventral spinocerebellar
  • cuneocerebellar
  • rostral spinocerebellar
19
Q

dorsal spinocerebellar tract

  • type of info
  • body parts
  • arises from
A

reafference info for legs and trunk, from Clarke’s nucleus

20
Q

ventral spinocerebellar tract

  • type of info
  • body parts
  • arises from
A

efference copy info for legs/trunk, from ventral horn

21
Q

cuneocerebellar tract

  • type of info
  • body parts
  • arises from
A

reafference info for arms from external cuneate nucleus

22
Q

rostral spinocerebellar tract

  • type of info
  • body parts
  • arises from
A

efference copy info for arms from ventral horn

23
Q

what are complex spikes?

A

neuron’s membrane voltage increases rapidly, but stays elevated for extended period of 20+ milliseconds

  • while potential is elevated, can fire ~5 APs in 1:1 relationship w/ arrival of APs on climbing fibers
  • -thus, single AP from inferior olive causes profound and long-lasting depolarization in membrane potential of Purkinje cell
  • typically occurs once/twice per second, and reliably produced by stimuli to distinct patches of skin
24
Q

what are error/unexpected signals in regards to complex spikes?

A

complex spiking can be related to the occurrence of unexpected stimuli

25
Q

what is the long term depression of complex spikes?

A

during and after complex spike (after-hyperpolarization), Purkinje cell is refractory to parallel fiber activation
-cellular basis for cerebellar learning

26
Q

what are the differential effects of parallel fibers and climbing fibers on Purkinje cells?

A

parallel fibers: simple spikes, 50-100 Hz

climbing fibers: complex spikes, 2-10 Hz, with strong synapse

27
Q

what are common symptoms of cerebellar lesions?

A
asthenia (loss of muscle strength)
atonia (loss of muscle tone)
-usually involve arms, occasionally legs
ataxia (decreased coordination and voluntary movements); most conspicuous
rebound disorder
oculomotor disorders
postural disorders
scanning speech
28
Q

what happens to cerebellar lesion patients when they try to coordinate movement?

A

since they have ataxia, they often show asynergia (difficulty coordinating muscle actions) and decomposition of movement (normal complex movements become broken down into single movements w/ single joints

29
Q

what happens to cerebellar lesion patients when they try to execute movement?

A

suffer from dysmetria (poorly directed movements), poorly directed movements that miss their targets, and deviations from the line of movement (doesn’t follow shortest path between points)
-intention tremor related to dysmetria, when involuntary shaking of reaching hand/limb as it performs action

30
Q

what happens when patients with cerebellar damage try to touch their nose with one finger?

A
  • movement becomes decomposed, b/c need coordinated movements of shoulder, elbow, and hand; instead does this individually
  • when finger approaches nose, involuntary alternating contractions of hand/wrist muscles cause finger to undershoot/overshoot nose
31
Q

what forms the basis of the modern sobriety test?

A

that high levels of alcohol consumption causes same effects as cerebellar lesions, b/c the cerebellum is affected first

32
Q

what id sysdiadochokinesia?

A

difficulty performing rapidly alternating movements seen in cerebellar patients
-movements of affected limb slow down and decrease in amplitude

33
Q

how are midline cerebellar lesions and ethanol intoxication similar to lateral cerebellar lesions?

A

both lead to oculomotor and postural disorders, analagous to weakness and dysmetria of limbs

  • difficulty maintaining gaze on moving objects and display nystagmus
  • scanning speech where articulation is problematic and staccato
34
Q

how are functions of cerebellum organized?

A

somatotopically

  • regions of cerebellum concerned with sensation/movement of arms, legs, eyes, and face are largely separate from each other
  • true even though these body parts are represented multiple times throughout cerebellar cortex, output nuclei, and targets of output nuclei
35
Q

what is the cerebellum’s contribution to experience-dependent modification of saccadic eye movements?

A

if there’s partial sectioning of left lateral rectus tendon

  • patch on left eye: right eye has normal movement, but left cannot reach target
  • patch on right eye: right eye overshoots, but left eye can very slowly made it to target
  • patch on right for 5 days: right eye still overshoots (but more fluidly) and left eye can reach target fluidly and as easily as right eye originally

this shows that the cerebellum can use error signals to adaptively modify commands for movement to optimize outcomes

36
Q

what are examples of cerebellar insults that produce cerebellar damage and cognitive deficits?

A
  • chronic dilantin medication
  • autism
  • schizophrenia
  • chronic alcohol abuse (thiamine deficiency)
37
Q

what is an essential tremor?

A

excess activity of inferior olive disrupts Purkinje cells w/ complex spiking that leads to dampening of deep nuclei output, followed by after hyperpolarization that promotes DN output

  • distinguished from Parkinson’s by L-DOPA and ethanol
  • can be treated by ethanol or barbituate administration, or deep brain stimulation (to eliminate cerebellar modification of motor commands)
38
Q

do lesions in cerebellum produce loss of function?

A

NO

-produce impairments in quality of movements and other functions, but it’s NOT a loss of function