Lecture 13: Basal ganglia Flashcards

1
Q

Label the basal gaglia and point out what two are actually joined together in a lot of animals?

A

Together the Caudate nucleus and putamen make the striatum

The external capsule travels between the putamen and Claustrum

The claustrum is a sheet of gray matter that is used for visual attention

Outside the Claustrum is the extreme capsule that separates the neocortex =(isulacortex resposible for GI system) and the claustrum

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2
Q

Pathway from the planning centre to the muscles?

A

Plannining via Glutamate(+) too

Striatum and then via GABA(-) too

  1. Substantia Nigra
  2. GPE (indirect)
  3. GPI (direct)

From GPE to the Subthalamic nucleus (SUT) via GABA

From SUT to GPI via Glutamate

GPI to VA-VL of thalamus via GABA

Finally from VA-VL to planning via glutamate before discussion between the planning and PMC

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3
Q

Huntington’s disease affects?

A

The indirect pathway from the striatum to the GPE

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4
Q

Parkinson’s disease affects?

A

The dopamine firbres in the nigrostriatal pathway that normally hold the striatal fibres tonically active. If these aren’t held here then more and more glutamate come down and don’t fibre whilst also have toxic levels of glutamate.

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5
Q

Symptoms of Parkinson’s disease?

A
  1. emotionally flat
  2. bradykinesia (hypokinesia) - hard to get started
  3. tremour at rest - pill roll (not typically annoying)
  4. rigidity
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6
Q

Pathology and neurochemistry of parkinson’s?

treatment?

A

Loss of dopamine cells in the substantia nigra pars compacta (SNc)

Depletion of dopamine in the striatum leading to a hypoexcitability in the cortex.

Most common: Leva Dopa

Other treatment: cell transplantation + gene therapy

Surgery: pallidotomy, thalanotomy, (or in SUT), DPS

  • pallidotomy and thalanotomy done on one side only
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7
Q

Hintington’s disease symptoms?

A

Behavioral/cognitive changes

HYPERKINESIA

Involuntary movements

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8
Q

Pathology and neurochemistry of Huntington’s?

Treatment?

A

Loss of GABAergic projection neurons in the striatum to the GPE leading to an increase in inhibition of the Glutamatergic (+) fibres going to the GPI. This results in a decreased inhibition (GABA) on the VA-VL leading to increased glutamate (+) firing to the planning cortex.

Genetic disease that is aquired but experiences genetic anticipation as males pass on a longer chain and females pass on a smaller chain normally. The length of the faulty chain determines the onset age.

Major treatment is for the associated depression but dopamine modulators are in phase III at the moment.

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