Basal Ganglia

Question 1

Basal Ganglia input/output

Answer 1

no direct sensory input or descending spinal pathway, modulates motor performance
input: from cerebral cortex
output: to cerebral (motor) cortex via thalamus
HUGE connections with cerebral cortex
MAJOR ROLE: motor program selection

Question 2

Dysfunction

Answer 2

Nontraumatic metabolic dysfunction as so much synthesis of NT happens here
Marked by motor “organization” problems
As with cerebellum, not sensory or strength impairment
DEFECTS ARE CONTRALATERAL unlike cerebellum

Question 3

Location

Answer 3

mass of grey matter at base of cerebrum, next to but not including thalamus

Question 4

Components (nuclei)

Answer 4

caudate and putamen (striatum), globus pallidus, substantia nigra, subthalamic nucleus

Question 5

Flow

Answer 5

cortex axons synapse in BG and release GLU –> (input to) GLU excites caudate and putamen (closest to cortex) –> release GABA to inhibit globus pallidus (output) –> also release GABA to inhibit thalamus –> back to cortex (so like a feedback loop for cortex)
[substantia nigra (striatum + thalamus) and subthalamic nucleus (pallidus) act as internal feedback loops)

Question 6

Medium Spiny Neurons

Answer 6

In striatum, project to:
D1 –> GPi (direct)
D2 –> GPe –> STN –> GPi (indirect)

Question 7

Nucleus Accumbens

Answer 7

caudal juncture between caudate and putamen

Question 8

Caudate and Putamen inputs

Answer 8

C: frontal association cortex and frontal lobes
P: Sensori-motor cortex

Question 9

Basal Ganglia activates motor control by …

Answer 9

… release from inhibition (disinhibition) NOT excitation
THE ESSENTIAL OUTPUT OF BG IS INHIBITORY (preventing thalamic excitation of cortex)
Without cortical input, the globus pallidus is spontaneously firing and thus inhibiting thalamic excitation of cortex, with cortical input the striatum is excited thus inhibiting the GP and thus freeing the thalamus from inhibition) THIS IS THE DIRECT PATHWAY (allows movement)

Question 10

Parkinson’s etiology

Answer 10

Loss of DA neurons in SN
As DA is excitatory to striatal neurons, there is less effective disinhibition, therefore motor actions are harder to get started (hallmark of Parkinson’s)

Question 11

Athetosis and Chorea

Answer 11

Both due to striatal damage:
Chorea - “dance” (usually distal) rapid, continuous
Athetosis - slow, writhing, ceaseless (hand, lips, tongue, neck, foot)

Question 12

Huntington’s

Answer 12

Chorea –> 10-15 years later dementia
CAG repeat (codes polyglutamine) in excess of 40 times
Loss of striatal action on GP

Question 13

Dopamine axis

Answer 13

Too little: rigidity, Parkinsonian symptoms

Too much: hyperkinesia

Question 14

Hemiballismus

Answer 14

Stroke in small ganglionic branch of PCA, damages subthalamic nucleus therefore inhibitory outflow of GP reduced and thalamus is able to excite cortex –> leads to inappropriate movement
No treatment