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Unit 4 > Basal ganglia > Flashcards

Basal ganglia Flashcards

1
Q

Components of the basal ganglia

A
  • Striatum (caudate, putamen)
  • Globus pallidus
  • Substantia nigra
  • Subthalamic nucleus
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2
Q

Dominant cell in the striatum

A

-Medium spiny stellate neurons

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3
Q

Inputs, outputs, and markers of medium spiny stellate neurons in the striosome

A
  • Inputs: Limbic cortex, Substantia nigra- pars compacta (SNpc)
  • Outputs: SNpc
  • Markers: GABA, no ACh
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4
Q

Inputs, outputs, and markers of medium spiny stellate neurons in the matrix

A
  • Inputs: cortex, interneurons, SNpc
  • Outputs: GPe and GPi
  • Markers:GABA, D2, ACh
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5
Q

Input structures of the basal ganglia

A
  • Striatum and subthalamic nucleus

- Direct projections from the cortex

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6
Q

Output structures of the basal ganglia

A
  • Globus pallidus internal (GPi)
  • Substantia nigra pars reticulada (SNpr)
  • Project back to the cortex via the thalamus
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7
Q

Intermediate structures of the basal ganglia

A
  • SNpc

- Subthalamic nucleus

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8
Q

Cortico-basal ganglia circuits bike analogy

A
  • Idea initiated in the cortex (pedals)
  • Idea translated to the input layer of the basal ganglia (front sprocket)
  • Chain passes to the output layer (rear break, always on)
  • Then passed to thalamus (rear sprocket)
  • SPpc cells (dopamine) keep the chain moving
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9
Q

Direct cortical-basal ganglia-thalamo-cortical circuit

A

-Cortex to striatum: excitatory projection
(at this point D1 from SNpc also contributes to excitatory projection)
-Striatum to GPi/SNr: inhibitory projection
-GPi/SNr to thalamus: Inhibitory projection
-Thalamus to cortex: Excitatory projection

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10
Q

Indirect cortical-basal ganglia-thalamo-cortical circuit

A

-Cortex to striatum: excitatory projection
(at this point D1 from SNpc contributes an inhibitory projection)
-Striatum to GPe: Inhibitory projection
-GPe to STN: Inhibitory projection
-STN to GPi/SNr: Excitatory projection
-GPi/SNr to thalamus: Inhibitory projection
-Thalamus to cortex: excitatory projection

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11
Q

Parallel segregated basal ganglia loops

A
  • Basal ganglia loops are anatomically segregated and distinct
  • Influence essentially all functions
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12
Q

Motor loop

A

-Motor cotex–>putamen–>lateral GP, internal segment–>ventral lateral and ventral anterior nuclei

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13
Q

Oculomotor loop

A

-Posterior parietal prefrontal cortex–>body of caudate–>GPi, SNpr–>mediodorsal and ventral anterior nuclei

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14
Q

Prefrontal loop

A

-Dorsolateral prefrontal cortex–>anterior caudate–>GPi, SNpr–>mediodorsal and ventral anterior nuclei

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15
Q

What is activated during difficult planning and visuomotor control?

A

-Basal ganglia–Globus Pallidus

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16
Q

Hyperdirect path

A
  • Allows cortex to directly excite the subthalamic nucleus, bypasses the striatum
  • Uses excitatory glutamine
17
Q

Striosomal path

A
  • Involved in habit learning
  • Giant cholinergic interneurons–tonically active neurons (TANs)
  • Interact with DA inputs of SNpc at the level of medium spiny stellate neurons (ACh enhances dopamine release)
  • Activated by rewards–part of neural substrate underlying behavioral reinforcement
18
Q

Hyperkinetic disorders

A
  • Abnormally low levels of BG output (disinhibits the thalamus)
  • Excessive motor activity
  • Huntington’s, sydenham’s,athetosis, hemmiballismus, dystonia, tourettes
19
Q

Hypokinetic disorders

A
  • Excessive inhibition of the thalamus by the BG
  • Impairment of initiation of movement (akinesia)
  • Reduction in the amplitude and velocity of movement (bradykinesia)
  • Parkinson’s
20
Q

Sydenham’s chorea

A
  • Caused by autoimmune reaction to childhood infection with group A B-hemolytic streptococci (occurs in 25% of patients with acute rheumatic fever)
  • Recovery in 50% of cases in 2-6 month
  • Striatum is the site of attack
  • aka PANDAs
21
Q

Huntington’s disease

A
  • Autosomal dominant
  • Atrophy of neostriatum especially the enkephalin-expressing neurons in the caudate
  • HD kills ENK neurons in the striatum which leads to unchecked D1 tone–increases drive to M1–hemiballistic movements
22
Q

Cells impacted in Parkinson’s

A
  • Locus coeruleus cells die first, then pars compacta cells

- Loss of dopamine causes a hyperactive break which impairs and slows movement

23
Q

Huntington’s treatment

A
  • Block excess action of direct pathway

- Anti-dopaminergic or dopamine-depleting drugs: haldol, olanzapine, tetrabenazine

24
Q

Parkinson’s treatment

A
  • Dopa won’t cross BBB so give L-DOPA
  • Only helps in the short term–can cause abnormal movements and/or hallucinations
  • Dopamimetics
  • MAO-B/COMP inhibitors–prevent degradation of DA
  • Anti-cholinergics
  • Palllidotomy or thalamotomy
  • Fetal nigral transplantation
  • Deep brain stimulation

Unit 4 (17 decks)

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