Basal Ganglia

Question 1

Function of basal ganglia

Answer 1

“mood and movement”
Initiation
Execution
Tone

Question 2

Components

Answer 2

Striatum: caudate nucleus and putamen
GP: internus and externus
Subthalamic nucleus
Substantia Nigra (midbrain) (pars reticulata, pars compacta)

Question 3

What connects the cortex to the striatum?

DIAGRAM

Answer 3

Corticostriate fibres, are excitatory so use glutamate

Question 4

What ouputs does the striatum have?

Answer 4

Striatopallidal fibres (externus!) and striatonigralfibres (SNr), both inhibitory so use GABA

Question 5

What output does the subtantia nigra have?

Answer 5

Nigrostriatal fibres, use dopamine.
Excitatory D1 receptors at the striatonigral cells
Inhibitory D2 receptors at the Striatopallidal cells

Question 6

What interactions are there with the SUT?

Answer 6

GPe inhibitory GABA fibres to the SUT

SUT to GPi excitatory glutamate fibres

Question 7

What are the outputs of the GPi?

Answer 7

Inhibitory GABA fibres to the VA-VL thalamus and the reticular formation

Question 8

Thalamic output?

Answer 8

VA-VL excitatory glutamate fibres to motor cortex

Question 9

How will diseases of the basal ganglia present?

Answer 9

Mood/cognitive changes
Difficulty initiating movements
Involuntary movements
Muscle tone defects

Question 10

Parkinsons symptoms

Answer 10

Emotionally flat
Bradykinesia/hypokinesia
tremor at rest
rigidity

Question 11

Pathology of Parkinsons

In terms of basal ganglia circuit

Answer 11

Loss of dopamine producing cells in SNc, meaning dopamine depletion in striatum.

Loss of nigrostriatal pathway, loss off dopamine; less inhibition of striatopallidal pathway to GPe so GABA accumulates; GABA inhibits the GPe to SUT pathway, decreasing GABA in the SUT; increased firing of SUT to GPi, increase of glutamate; going to cause GPi to VA-VL to proudce lots of GABA; Inhibition of thalamus to motor cortex, reduced glutamate

Question 12

Treatments of parkinsons

Answer 12

• Replace the dopmaine lost with L-DOPA
• Thalamotomy, lesion in VA-VL thalamus
• Pallidomtomy, lesion of GPi
• Deep brain stimulation of SUT and GPi
• cell transplantation and gene therapy

Question 13

Huntingtons disease symptoms, pathology and treatment

Dominant gene on chromosome 4, increased glutmatae? cell death in striatum

Answer 13

Symptoms:

• Behaviorual/cognitive changes
• Hyperkinesia
• Involuntary movements

Patholgy: loss of inhibitory GABA fibres
Loss of GABA in GPe, more GABA in SUT, less glutamate in GPi, less GABA in VA-VL, more glutamate in motor cortex

treatment: symptomatic, gene therapy?,