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Basal Ganglia - Functions, Connections & Abnormalities

(Long Answer - 1st Year Physiology Exam)

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1. INTRODUCTION

Memory trick: "CAPS + SN" = Caudate, Amygdala, Putamen, (globus pallidus =) Striatum + Nigra

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2. COMPONENTS / ANATOMY

• Putamen + Globus pallidus = Lenticular nucleus
• ~95% of striatal neurons = medium spiny neurons (use GABA)
• Remaining = aspiny interneurons (use ACh, somatostatin, GABA)

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3. CONNECTIONS OF BASAL GANGLIA

INPUTS (Afferents)

1. Corticostriate pathway - from wide areas of cerebral cortex (especially motor cortex)
2. Thalamostriatal pathway - from intralaminar nuclei of thalamus

INTERNAL CIRCUITRY - TWO PATHWAYS

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A. DIRECT PATHWAY (Net = EXCITATORY → facilitates movement)

Cortex → Striatum → GPi/SNpr → Thalamus → Motor Cortex
         (GABA: inh) (GABA: inh)  (Glu: exc)

• Striatum inhibits GPi/SNpr (GABAergic)
• GPi/SNpr would normally inhibit thalamus - this inhibition is now REDUCED
• Thalamus is released from inhibition → excites motor cortex
• Result: Movement is FACILITATED

Memory trick: Direct = D for Dopamine facilitates (D1 receptors), D for Doing movement

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B. INDIRECT PATHWAY (Net = INHIBITORY → suppresses movement)

Cortex → Striatum → GPe → Subthalamic nucleus → GPi/SNpr → Thalamus → Motor Cortex
         (GABA:inh) (GABA:inh)  (Glu: exc)         (GABA:inh)   (Glu:exc)

• Striatum inhibits GPe (GABA)
• GPe would normally inhibit subthalamic nucleus - this inhibition is now REDUCED
• Subthalamic nucleus excites GPi/SNpr (Glu)
• GPi/SNpr inhibits thalamus (GABA) → motor cortex activity reduced
• Result: Movement is SUPPRESSED

Memory trick: Indirect = Inhibitory = I for Inhibiting movement

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C. DOPAMINERGIC PATHWAY (Nigrostriatal pathway)

• SNpc sends dopamine back to striatum
• Dopamine acts on D1 receptors → facilitates direct pathway (excitatory effect)
• Dopamine acts on D2 receptors → inhibits indirect pathway (also facilitates movement)
• Overall: Dopamine promotes movement

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OUTPUTS (Efferents)

1. GPi → Thalamus (via ansa lenticularis & lenticular fasciculus)
2. SNpr → Thalamus
3. GPi → Brainstem (pedunculopontine nucleus - PPN) → motor neurons in brainstem & spinal cord

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SUMMARY TABLE OF NEUROTRANSMITTERS

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4. FUNCTIONS OF BASAL GANGLIA

Memory trick: "PEACE" = Planning, Execution, Affective, Cognitive, Extrapyramidal

1. Planning & programming of voluntary movement - neurons discharge even before movement begins
2. Execution of smooth, coordinated movement - converts abstract thought into voluntary action
3. Maintenance of posture and muscle tone
4. Suppression of unwanted movements - via indirect pathway
5. Cognitive functions - caudate nucleus connected to prefrontal cortex; involved in object reversal, delayed alternation
6. Affective/emotional behavior - via amygdala connections
7. Language - lesion of left caudate nucleus → dysarthric aphasia resembling Wernicke's

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5. DISEASES / ABNORMALITIES OF BASAL GANGLIA

1. Nigrostriatal dopaminergic system
2. Intrastriatal cholinergic system
3. GABAergic system (striatum → globus pallidus/SN)

A. HYPOKINETIC DISORDERS (decreased movement)

PARKINSON'S DISEASE

• Cause: Degeneration of SNpc → loss of dopamine in striatum
• Effect: Direct pathway under-activated + Indirect pathway over-activated → thalamus excessively inhibited → reduced motor cortex activity
• Features (TRAP):
  • Tremor - resting ("pill-rolling") tremor, 4-6 Hz
  • Rigidity - cogwheel or lead-pipe rigidity
  • Akinesia/Bradykinesia - slowness/poverty of movement
  • Postural instability
• Treatment: Levodopa (L-DOPA) - replenishes dopamine

Memory trick: TRAP = Tremor, Rigidity, Akinesia, Postural instability

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B. HYPERKINETIC DISORDERS (excessive, abnormal movements)

HUNTINGTON'S DISEASE (Huntington's Chorea)

• Cause: Autosomal dominant, chromosome 4; loss of GABAergic neurons in striatum (especially those projecting via indirect pathway)
• Effect: Indirect pathway is impaired → excessive thalamic excitation → excess movement
• Features:
  • Chorea (rapid, involuntary, irregular, dance-like movements)
  • Progressive dementia
  • Psychiatric disturbances
  • Onset: 35-50 years

Memory trick: Huntington's = Hyperkinetic, Hereditary, chromosome 4 (4 letters in "Hunt")

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HEMIBALLISMUS

• Cause: Lesion of subthalamic nucleus (e.g., small hemorrhage/infarct)
• Effect: Loss of subthalamic excitation of GPi → GPi under-active → thalamus over-excited → excess movements
• Features: Violent, flinging movements of the contralateral limbs (especially proximal)
• Predominantly affects one side (hemi = one side)

Memory trick: Ballismus = like throwing a ball - violent flinging movement

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OTHER HYPERKINETIC CONDITIONS

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6. QUICK COMPARISON TABLE (Exam Favorite)

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7. MEMORY SUMMARY DIAGRAM

CORTEX (Glu, excitatory)
    ↓
STRIATUM
    |
    |--- DIRECT PATH (D1 receptor, dopamine facilitates)
    |    ↓ GABA (inhibit GPi)
    |    GPi inhibited → LESS inhibition of thalamus
    |    → THALAMUS excited → CORTEX excited → MOVEMENT
    |
    |--- INDIRECT PATH (D2 receptor, dopamine inhibits)
         ↓ GABA (inhibit GPe)
         GPe inhibited → LESS inhibition of subthalamic nucleus
         Subthalamic nucleus (Glu) → excites GPi
         GPi MORE active → MORE inhibition of thalamus
         → THALAMUS inhibited → CORTEX inhibited → NO MOVEMENT

SNpc ----[dopamine]---→ STRIATUM (maintains balance)

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KEY POINTS TO REMEMBER FOR EXAM

1. Basal ganglia = CAPS + SN (Caudate, Amygdala, Putamen, striatum = lenticular nucleus + Nigra)
2. Direct pathway = excitatory = facilitates movement (net result)
3. Indirect pathway = inhibitory = suppresses movement (net result)
4. Dopamine (from SNpc) promotes movement via D1 (direct) and D2 (indirect) receptors
5. GABA is the main inhibitory transmitter; Glutamate is excitatory throughout
6. Parkinson's = hypokinetic = dopamine LOSS in SNpc → treat with Levodopa
7. Huntington's = hyperkinetic = GABA loss in striatum → indirect pathway fails
8. Hemiballismus = subthalamic nucleus lesion → violent flinging movements

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