N375: basal ganglia

How do basal ganglia and cerebellum differ in movement control?

BG releases/initiates movement; cerebellum modulates/refines movement.

Laterality: basal ganglia vs cerebellum?

BG acts contralaterally; cerebellum acts ipsilaterally.

Basal ganglia main question?

“Should I start this movement?”

Cerebellum main question?

“How do I make this movement smooth and accurate?”

What nuclei make up the striatum?

Caudate + putamen.

What nuclei make up the lentiform nucleus?

Putamen + globus pallidus.

What are the two parts of the globus pallidus?

GPe (external) and GPi (internal).

What nuclei provide major output of BG?

GPi + SNr → VA/VL thalamus → motor cortex.

What neurotransmitters are balanced in the striatum?

Dopamine, GABA, acetylcholine.

What happens if dopamine–ACh–GABA balance is lost?

Movement disorders: PD, HD, dystonias, choreas.

What is the only excitatory intrinsic pathway in the BG?

STN → GPi (glutamatergic).

What are the basal ganglia?

collection of subcortical nuclei deep in the forebrain. receives constant input from cortex, outputs to prefrontal/supplementary/primary motor via thalamus

Direct pathway: purpose and mechanism?

GO—facilitates movement; D1 dopamine ↑ striatal firing → inhibits GPi/SNr → thalamus disinhibited → ↑ cortical output.

Indirect pathway: purpose and mechanism?

STOP—inhibits unwanted movement; D2 dopamine ↓ striatal firing → GPe less inhibited → STN activity controlled → GPi inhibits thalamus → ↓ cortical output.

What is the shared goal of both pathways?

Modulate how strongly GPi inhibits the thalamus.

Where do both pathways begin?

Cortex → glutamatergic input to striatum.

What promotes movement initiation?

Activate direct pathway + inhibit indirect (↑ dopamine).

What promotes stopping movement?

Inhibit direct pathway + activate indirect (↓ dopamine).

What neurotransmitter is lost in Parkinson’s?

Dopamine from SNc.

Classic movement features of PD?

Bradykinesia, poverty of movement, resting tremor (“pill-rolling”), ↑ muscle tone.

PD effect on direct pathway?

Less dopamine → less D1 activation → weak direct → GPi overactive → thalamus inhibited → ↓ movement.

PD effect on indirect pathway?

Less dopamine → D2 not inhibited → striatum overactive → more GABA to GPe → GPe suppressed → STN hyperactive → GPi hyperactive → thalamus suppressed → ↓ movement.

Why is paralysis not seen in PD?

CST is intact; problem is BG modulation, not motor neuron death.

What neurons degenerate in Huntington’s?

GABAergic striatal neurons of the indirect pathway.

HD effect on indirect pathway?

Weak/absent inhibition of GPe → GPe overactive → STN suppressed → GPi underactive → thalamus disinhibited → excessive movement.

Is the direct pathway mostly intact in HD?

Yes :D

Resulting symptoms of HD?

Chorea: involuntary flinging, twisting, dance-like movements.

What lesion causes hemiballismus?What lesion causes hemiballismus?

Destruction of the subthalamic nucleus (STN).

Why does STN loss cause extreme hyperkinesia?

STN cannot excite GPi → GPi fails to inhibit thalamus → unrestrained cortical drive → violent, ballistic movements.

How is hemiballismus different from HD?

HD = partial loss of indirect pathway; hemiballismus = complete STN knockout, more severe.

3 hallmark categories of BG lesion motor disturbances?

• Tremor/involuntary movements (dyskinesia, chorea)

• Abnormal muscle tone/posture

• Poverty of movement (without paralysis)

What is the final output of the BG and how is it normally acting?

GPi → GABA on thalamus → normally inhibitory.

What does dopamine do in striatum?

Excites D1 (direct) and inhibits D2 (indirect) → net more movement.