Lecture 3: Basal Ganglia Flashcards

1
Q

What are the 5 parts of the Basal Ganglia and what are they all made of. What is the striatum

A

All made of grey matter which contain many cell bodies
1. Caudate nucleus:
2. Putamen
3. Globus Pallidus (Intus/Extnus)
4. Subthalamic nucleus
5. Substantia nigra (pars compacta and pars reticulate)
Striatum is 1 + 2

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2
Q

Can you describe the Internal capsule, external capsule, extreme capsule, claustrum - relative location and possible function

A

Internal capsule is white matter tract separating the two parts of the striatum allowing passage of axons from cortex to thalamus

External capsule is white matter tract that divides the putamen from the claustrum (grey matter involved with visual attendance) which helps info to travel from ant to post.
- Extreme capsule is lateral to the claustrum. Lateral to this is cortical grey matter of the insular cortex and temporal operculum

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3
Q

What are the 3 functions of the Basal ganglia

A
  • coordinating fine motor control
  • express mood through movement
  • adjust a movement as it happens if movement is trained
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4
Q

What are the neurotransmitters and neural pathways in the basal ganglia circuit from initial input from cerebral cortex, to output to prefrontal, pre motor and motor cortices

A
  1. Excitatory neurons go from the cerebral cortex to the striatum, synapsing on 3 possible pathways (glutamate)

a) Indirect pathway: Striatum to GPE to SubThalN via inhib GABA. Then excitatory to GPI
b) Direct pathway: Striatum to GPI via inhib GABA
Which oppose each other to make input and output balance.
c) Striatum to SubNigra via inhib GABA

  1. Inhib fibre from internal GP goes to the ventral anterior-ventral lateral nucleus of the thalamus
  2. Excite fibre from Thalamus goes back to cerebral cortex (premotor planning part
  3. Activation of Upper motor neuron
  4. Dopaminergic fibre from substantia nigra to striatum- inhib or excite depending on receptor type. Primes the neurons in the striatum to fire.
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5
Q

What happens to the basal ganglia circuit in Huntingtons disease

A
  1. The nerves from the Striatum to the GPE die.
  2. So the nerves from the GPE to the subthalamic nucleus are uninhibited to fire so increase their inhibitory activity
  3. This increases inhibition on the excitatory fibre from subTN to the GPI.
  4. This means that the inhibitory neuron which usually fires to inhibit excitatory signals from the VAVL to Cerebral cortex doesn’t have its own excitation stimulus, only inhibitory stimulus so there is hyperexcitation in the Cortex–> Hyperactivity in the periphery.
  • There is also increased original glutamate input to the striatum leading to excitotoxicity

Later in the disease there is death of pathway to sub. nigra and then death to the direct pathway. Leading to parkinsons like disease- Hypo excitability.

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6
Q

What happens to the basal ganglia circuit in Parkinsons disease

A
  1. The sub niagra disappears so there is no more dopamine input to the striatum.
  2. 3 pathways from the striatum aren’t primed to fire so glutamate increases leading to excitotoxicity
  3. This means that there is no more input (excitatory or inhibitory) to the GPI nerve which is inhibitory to the VAVL Thalamus nerve
  4. This leads to increased inhibition of excitatory nerve to the cerebral cortex= hypoexcitation -> hypoactivity, difficulty in initiating movement.
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7
Q

‘What are the treatments available for Parkinsons

A

Levadopa which is the precursor to dopamine, converted by remaining subnigra cells. However peaks and troughs lead to depression, hallucination at peaks and muscle rigidity and executive function disorder and troughs.

Dopamine breakdown (maob) inhibitors

Deep brain stimulation putting a stimulator in to GPE,GPI (antidyskinesia), STN (anti parkinsonism)

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