The Basal Ganglia

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Lecture 12

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22 Terms

1
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What are the five major nuclei of the basal ganglia?

Caudate, putamen, globus pallidus (GPe/GPi), subthalamic nucleus (STN), substantia nigra (SNc/SNr).

2
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What structures make up the striatum?

Caudate, putamen, nucleus accumbens.

3
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What structures make up the lenticular nucleus?

Putamen + globus pallidus.

4
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What is the primary input nucleus of the basal ganglia?

Striatum.

5
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What is the primary output nucleus of the basal ganglia?

GPi and SNr.

6
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Are basal ganglia outputs inhibitory or excitatory?

Inhibitory (GABAergic).

7
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Which pathway facilitates movement?

Direct pathway.

8
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Which pathway inhibits movement?

Indirect pathway.

9
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What neurotransmitter does the substantia nigra pars compacta release?

Dopamine

10
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What receptors does dopamine activate in the direct vs. indirect pathway?

D1 = excitatory (direct), D2 = inhibitory (indirect).

11
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What happens in Parkinson’s disease?

Degeneration of SNc dopaminergic neurons.

12
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What are common symptoms of PD?

Bradykinesia, rigidity, tremor, akinesia.

13
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Name all major basal ganglia nuclei and describe their general roles.

  • Caudate nucleus: cognitive/oculomotor functions; input to BG.

  • Putamen: sensorimotor input; main motor-related input region of striatum.

  • Globus pallidus:

    • GPe: regulates indirect pathway.

    • GPi: major output nucleus.

  • Subthalamic nucleus (STN): excitatory drive to GPi (glutamate).

  • Substantia nigra:

    • SNc: dopamine → modulates striatum (D1/D2).

    • SNr: output nucleus (similar to GPi).

14
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Describe the main afferent connections into the striatum.

  • Corticostriatal: from all cortical areas (glutamate).

  • Thalamostriatal: from intralaminar nuclei (glutamate).

  • Nigrostriatal: from SNc (dopamine).

15
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Describe the major efferent connections of the basal ganglia.

Outputs are inhibitory (GABA) and arise from:

  • GPi → thalamus (VA/VL/DM) → motor cortex.

  • SNr → thalamus, brainstem gaze centers.

16
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Describe the motor loop through the basal ganglia.

Motor/association cortex → striatumGPi/SNrVA/VL thalamusmotor cortex (M1/SMA).
Basal ganglia do NOT initiate movement, but select, reinforce, or suppress motor programs.

17
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Describe the direct pathway (step-by-step).

  • Cortex excites striatum (glutamate).

  • Striatum inhibits GPi/SNr (GABA).

  • GPi/SNr inhibition → releases thalamus from inhibition (“disinhibition”).

  • Thalamus excites motor cortex → movement promoted.

18
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Describe the indirect pathway (step-by-step).

  • Cortex excites striatum.

  • Striatum inhibits GPe.

  • Reduced GPe activity → less inhibition of STN.

  • STN becomes more active → excites GPi/SNr.

  • GPi/SNr increases inhibition on thalamus.

  • Thalamus cannot excite cortex → movement inhibited.

19
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Explain how dopamine affects the direct & indirect pathways.

  • D1 receptors (direct): dopamine excites → increases movement.

  • D2 receptors (indirect): dopamine inhibits → reduces indirect pathway → increases movement.
    Net effect = promotes movement.

20
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List the four basal ganglia circuits and their functions.

  • Motor loop: learned movements and execution.

  • Cognitive loop: planning, working memory.

  • Limbic loop: emotional/motivational aspects of movement.

  • Oculomotor loop: voluntary saccadic eye movements.

21
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Describe the basal ganglia changes in Parkinson’s disease.

  • Loss of dopaminergic neurons in SNc.

  • Decreased direct pathway activity (less D1 stimulation).

  • Increased indirect pathway activity (less D2 inhibition).

  • Increased GPi/SNr output → excessive thalamic inhibition.

  • Hypokinetic symptoms: bradykinesia, rigidity, resting tremor, shuffling gait.

22
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What disorders arise from excessive movement (hyperkinesia)?

  • Chorea: rapid, jerky movements (Huntington’s).

  • Athetosis: slow, writhing movements.

  • Ballismus: violent flinging of limbs (STN lesion).

  • Tremor: resting or intention.