Lecture 12: Movement II - Basal Ganglia Flashcards

1
Q

What is hyperalgesia, and what is an example?

A
  • Peripheral sensitization to pain after damage

- Increased sensitivity to temperature after sunburn

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2
Q

What does the ciliary body do?

A
  • Produces fluid to fill the front of the eye
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3
Q

What are the functions (2) of the retinal pigment epithelium?

A
  • Phagocytosis of shed outer segments

- Regeneration of the photoreceptor pigments

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4
Q

What does the lateral corticospinal innervate?

A
  • Alpha motor neurons that are important for writing
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5
Q

What is the monocular portion of the visual field represented by on the retina?

A
  • Nasal portion
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6
Q

Axons of upper motor neurons that supply lower motor neurons for skilled movements can be found in…

A
  • Lateral white matter
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7
Q

What are the horns made up of?

A
  • Grey matter/cell bodies
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8
Q

What is the white matter?

A
  • Tracts

- Lots of myelin

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9
Q

Applying a drug that increases cGMP levels in photoreceptors would cause __________ in response to photon of light.

A
  • Attenuated hyperpolarization
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10
Q

What is the basal ganglia responsible for, in general?

A
  • Initiation of intended movement and suppression of unwanted movement
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11
Q

What is the basic function of the basal ganglia?

A
  • To influence movement by regulating activity of UMNs (no direct action on LMNs)
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12
Q

When does the basal ganglia modulate UMN activity?

A
  • In anticipation of and during movement
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13
Q

What/where is the basal ganglia?

A
  • Diverse set of nuclei deep in cerebral hemispheres
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14
Q

What structures does the basal ganglia include?

A
  • Caudate nucleus (striatum)
  • Putamen (striatum)
  • Globus Pallidus (internal and external capsules)
  • Subthalamic nucleus
  • Substantia nigra
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15
Q

What are the major components that receive and process movement-related signals?

A
  • Striatum (caudate nucleus and putamen) and pallidum (globus pallidus and substantia nigra pars reticulata)
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16
Q

Where does the substantia nigra pars compacta send signals to?

A
  • Striatum
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17
Q

Where does the subthalamic nucleus send inputs to?

A
  • Pallidum
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18
Q

What do subcortical loops link?

A
  • Link most areas of cerebral cortex with UMNs in premotor and primary motor cortices via thalamus
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19
Q

What does the SNc have a strong connection with?

A
  • Dorsal striatum
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20
Q

What is the nucleus accumbens responsible for?

A
  • Reward and reinforcement
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21
Q

Describe the body movement loop?

A

Motor/premotor/somatosensory cortices -> Putamen -> Lateral globus pallidus/internal segment -> Ventral lateral and ventral anterior nuclei of thalamus -> primary motor/premotor/supplementary motor cortex

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22
Q

Describe the oculomotor loop?

A

Posterior parietal/prefrontal cortex -> Caudate (body) -> Globus pallidus/internal segment, SNr -> Mediodorsal and ventral anterior nuclei -> Frontal eye field/supplementary eye field

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23
Q

What are the 2 main input nuclei of basal ganglia?

A
  • Caudate

- Putamen

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24
Q

Where do the caudate and putamen receive projections from?

A
  • Nigrostriatal (SNc)

- Corticostriatal (parietal, frontal, temporal, occipital lobes of cortex)

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25
Q

Where, specifically, does the caudate receive cortical projections from?

A
  • Primarily from multimodal association cortices

- Frontal mediated eye movements (where you orient attention)

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26
Q

Where, specifically, does the putamen receive cortical projections from?

A
  • SI, SII somatosensory cortices
  • Primary motor cortex
  • Higher order visual cortices
  • Auditory association cortices
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27
Q

What are medium spiny neurons?

A
  • Have large dendrites
  • A lot of dendritic branching
  • Good example of convergence
  • Part of striatal internal circuitry
28
Q

Where do medium spiny neurons receive convergent input from?

A
  • Cortical neurons
  • Dopaminergic projections from SNc
  • Modulation via local circuit neurons
29
Q

Where do medium spiny neurons project to?

A
  • Other basal ganglia regions
  • Segregated outputs
  • Primarily globus pallidus and SNr
30
Q

Where does the putamen project to?

A
  • Internal Globus Pallidus (GPi)

- External Globus Pallidus (GPe)

31
Q

Where does the caudate project to?

A
  • Internal Globus Pallidus (GPi)

- Substantia nigra pars reticulata (SNr)

32
Q

What is medium spiny neuron firing related to?

A
  • Impending movement
  • Intention to move
  • Also related to termination/suppression of unwanted movements
  • Could also be related to initiation of new movement
33
Q

What are the primary output nuclei for MSNs of striatum?

A
  • GP and SNr
34
Q

What type of neurons are MSNs?

A
  • Inhibitory (GABAergic)
35
Q

Where does the GPi project to?

A
  • Ventral anterior and ventral lateral thalamus (VA/VL complex)
36
Q

Where does the VA/VL complex project to?

A
  • Upper motor neurons in motor cortex and brainstem
37
Q

Where does the SNr project to?

A
  • Superior colliculus
  • Command head/eye movements
  • Bypassing the thalamus
38
Q

What type of pathways do MSNs project onto?

A
  • Pathways with high spontaneous activity to tonically inhibit (continually suppressing) cells in the superior colliculus of thalamus
  • Increases inhibitory output from striatum suppresses tonic inhibition, releasing activity in superior colliculus and thalamus and allowing activation of UMNs
39
Q

What happens when the striatum is at rest?

A
  • Globus pallidus is tonically active
  • VA/VL complex of thalamus is inhibited
  • There is no excitation of motor cortex
40
Q

What happens when the striatum is transiently excited?

A
  • Globus pallidus is transiently inhibited
  • VA/VL complex of thalamus is disinhibited so other inputs can excite it
  • Leads to excitation of motor cortex
41
Q

What is the direct pathway?

A
  • Release of thalamocortical circuits from tonic inhibition

- Works to decrease inhibitory output from GPi to VA/VL (disinhibition)

42
Q

What is the indirect pathway?

A
  • Antagonizes activity of direct pathway via GPe and the subthalamic nucleus
  • Increases level of tonic inhibition provided by GPi
  • Works to increase inhibitory output from GPi to VA/VL
43
Q

What kind of path is the D1 receptor part of?

A
  • Direct path

- Excitatory

44
Q

What type of path is the D2 receptor a part of?

A
  • Indirect path

- Inhibitory

45
Q

How do disorders of movement occur?

A
  • Elements of basal ganglia loops are dysregulated
  • Motor systems cannot switch smoothly b/n initiation and termination
  • Movements can be a consequence of maladaptive UMN activity
46
Q

What is the main inhibitory neurotransmitter in the adult brain?

A

GABA

47
Q

Dopaminergic neurons that synapse on MSNs originate in which brain region?

A

Substantia nigra pars compacta

48
Q

What is the transmitter for the medium spiny neurons of the striatum?

A

GABA

49
Q

Where do SNr axons project to that globus pallidus axons do not?

A

Superior colliculus

50
Q

What is Parkinson’s Disease?

A
  • Specific degeneration of dopamine projection neurons from the SNc
51
Q

Under standard circumstances, what does release of dopamine into the striatum do?

A
  • Increase responsiveness of direct pathway to cortical input (via D1 activation)
  • Decreases responsiveness of indirect pathway (via D2 activation)
  • Need to be able to signal MSNs
52
Q

How does Parkinson’s disease affect the direct pathway?

A
  • Less excitation of C/P inhibition on GPi -> greater tonic inhibitory activity of GPi -> More inhibition of VA/VL -> Less activation of motor cortices
53
Q

How does Parkinson’s disease affect the indirect pathway?

A
  • Less inhibition of C/P inhibition of GPe -> Less inhibition on STN -> Greater excitation of GPi -> More inhibition of VA/VL -> Less activation of motor cortices
54
Q

Once behaviour has been initiated, what might UMNs be able to do?

A
  • Maintain behaviour without input from basal ganglia
55
Q

What is the effect of cycling in some Parkinson’s patients?

A
  • Improvement in motor function that lasts for weeks

- Perhaps strengthening circuitry between UMNs and LMNs

56
Q

What is Huntingdon’s disease?

A
  • Initially specific degeneration of striatal MSNs that project to the GPe that gradually atrophies the entire caudate and putamen
57
Q

What is the effect of Huntingdon’s disease in the basal ganglia?

A
  • Loss of inhibitory C/P MSN projections to GPe -> Greater inhibition on STN -> Less excitation on to GPi and increased direct inhibition from GPe -> Less inhibition of VA/VL -> More activation of motor cortices
  • UMNs can be activated by inappropriate signals without influence of basal ganglia
58
Q

What is hyperkinesis?

A
  • Too much unwanted movement
59
Q

Which cortices send input to basal ganglia?

A
  • Motor
  • Association
  • Sensory
60
Q

Afferents that go to putamen come from where?

A
  • Motor and sensory cortices
61
Q

What pathway are movements facilitated through?

A
  • Direct pathway
62
Q

Which pathway are competing movements inhibited through?

A
  • Indirect pathway
63
Q

Where is the caudate nucleus located?

A
  • Floor of anterior horn of lateral ventricle
64
Q

Where is the substantia nigra located?

A
  • Cerebral peduncles of midbrain
65
Q

Where do dopaminergic neurons project to?

A
  • Caudate/putamen

- Influence motor output

66
Q

What does the subthalamic nucleus act as?

A
  • Pacemaker for basal ganglia circuitry through inhibitory influences