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U5 Neuroscience > Basal Ganglia and Movement Disorders > Flashcards

Basal Ganglia and Movement Disorders Flashcards

1
Q

What are the 4 structures of the basal ganglia?

A
  • substantia nigra
  • striatum
  • globus pallidus
  • subthalamic nuclei
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2
Q

Which part of the substantia nigra produces dopamine?

A

pars compacta (SNpc)

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3
Q

Where are medium spiny stellate neurons in the basal ganglia?

A

striosome, matrix

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4
Q

What are the input structures of the basal ganglia? What do they receive direct projections from?

A

striatum, also subthalamic nuclei (via hyperdirect path)

cerebral cortex

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5
Q

What are the output structures of the basal ganglia? What do they project to?

A

globus pallidus internal segment (GPi), substantia nigra pars reticula (SNpr)
thalamus (which projects back to cortex)

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6
Q

What are the intermediate structures of the basal ganglia? What do they modulate?

A

SNpc, STN

modulate activity of input and output structures

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7
Q

What does the direct pathway disinhibit? What is the effect on cortical activity?

A

disinhibits the thalamic output neuron, which excites the cortex

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8
Q

What does the indirect pathway disinhibit? What is the effect on cortical activity?

A

disinhibits the STN neuron, which excites the GPi brake

decreases thalamic feedback to cortex, inhibitory

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9
Q

Is the output layer cell (GPi) always inhibitory to the thalamus?

A

yes

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10
Q

What is the effect of the indirect pathway on the brake? on thalamic neurons?

A

ramps up the brake, inhibits excitatory thalamic neurons

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11
Q

What is the effect of the direct pathway on the brake? on thalamic neurons?

A

inhibits the brake, excites the excitatory thalamic neurons

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12
Q

What does the STN neuron receive input from?

A

GPe neuron in indirect path, direct projection from cortex

both have the end effect of exciting the STN neuron to ramp up the brake

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13
Q

How does dopamine affect the direct pathway?

A

acts on excitatory D1 receptors to ramp up the direct path to turn off the brake

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14
Q

How does dopamine affect the indirect pathway?

A

acts on inhibitory D2 receptors to turn off the indirect path to turn off the brake

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15
Q

What shuts off the indirect path and activates the direct path? How does it do two separate effects?

A

dopamine through D1 and D2 receptors

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16
Q

What are GP neurons involved in nonmotor loops involved in? Where are they located in the GP? What area of cortex are the related to?

A

short term and working memory, located in dorsomedial GP, receive input from and project back to prefrontal cortex

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17
Q

What are GP neurons involved in motor loops involved in? Where are they located in GP? What area of cortex are they related to?

A

motor tracking, located in ventral GP, receive input from and project back to motor areas

18
Q

Where is activity in GP for visually guided tracking task?

A

track neurons are ventral

19
Q

Where is activity in GP for remembered sequence tasks?

A

REM (remember) neurons are dorsomedial

receive input from SMA (associated with sequential motor performance) and prefrontal area

20
Q

What area is activated in Tower of London task?

A

dorsomedial GP because it involves higher order control, planning and cognition

21
Q

What is the hyperdirect path?

A

from cortex to STN, ramps up brake

22
Q

What is the striosomal path? What does it cause the release of?

A

from cortex to MSSNs in striatum that project to SNpc (don’t participate in direct or indirect path)
causes release of DA from reward cortical areas

23
Q

What neurons are involved in habit learning?

A

cholinergic TANs (tonically active neurons), dopaminergic neurons and MSSNs in striatum

24
Q

When are SNpc and TAN activated by motor cues?

A

only when the movement is motivated by rewards (reward based shaping of neuronal activity)

25
Q

How do TANs participate in reward based shaping of neuronal activity?

A

Ach release increases release of DA whenever dopaminergic neurons are firing (since TANs are tonically active will fire with the DA neurons to get conditioned)

26
Q

What is hyperkinetic dysfunction of basal ganglia caused by?

A

abnormally low levels of basal ganglia output, brake is abnormally turned off

27
Q

What are some hyperkinetic disorders?

A

huntingtons, syndenham’s chorea, hemiballism

28
Q

What is hypokinetic dysfunction of basal ganglia caused by?

A

excessive levels of basal ganglia output, brake is abnormally turned on

29
Q

What is the major hypokinetic disorder? What causes it? What are the symptoms?

A

Parkinsons
loss of SNpc DA-producing cells
akinesia, bradykinesia, resting tremor, deadpan face

30
Q

What is chorea?

A

dance-like, quick jerky purposeless movements

primarily involves distal muscles of extremities

31
Q

What is Sydenham’s chorea?

A

autoimmune reaction to group A strep

autoantibodies react with striatum and attack cells in indirect path

32
Q

What pathway does Huntington’s target?

A

indirect path, cells in this path express different neuropeptides suscpetible to the mutation

33
Q

What are the higher order/extra motor consequences of basal ganglia damage in Huntingtons? sydendham’s chorea? parkinsons?

A

huntingtons- cognitive deficits, dementia
sydenham’s chorea- emotional, behavioral deficits, OCD
parkinsons- dementia in advanced stages

34
Q

Why does carbon monoxide poisoning affect basal ganglia?

A

big metabolic sink because of tonically active cells, causes pathology because basal ganglia isn’t getting oxygen

35
Q

How do wasp stings affect basal ganglia?

A

due to autoantibodies attacking basal ganglia

36
Q

How do you treat Huntingtons?

A

block excessive action of direct path with anti-DA drugs

37
Q

How do you treat Syndenham’s chorea?

A

antibiotics for the strep, immunosuppressants against the autoantibodies, plasmapheresis

38
Q

How do you treat Parkinson’s with meds (4)?

A

L-DOPA (because DA is too big to cross BBB and will have peripheral effects)
dopamimetics, MAO-B inhibitors to prevent DA degeneration, anticholinergics to dampen unregulated DA release to help tremor

39
Q

What are side effects of LDOPA?

A

dyskinesias (increased drive to primary motor cortex), hallucinations (increased drive to TE) from overexcitation of thalamus

40
Q

How do you treat Parkinson’s surgically?

A

lesion GPi or VL thalamus, if brake is overactive destroy the brake
put DA-producing cells back in (fetal nigral tissue)
deep brain stimulation to pacemake STN to force normal rhythm of discharge

U5 Neuroscience (35 decks)

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