10 Basal Ganglia II Flashcards

1
Q

what are the main inputs to the basal ganglia? what about outputs?

A

inputs: striatum
outputs: globus pallidus, SNR

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2
Q

in the resting state, what does the basal ganglia do the the thalamus?

A

The basal ganglia suppress movement by inhibiting the thalamus and ultimately the cortex

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3
Q

What is the function of the internal basal ganglia circuits?

A

to connect the input side (striatum) to the output sides (GPi and SNR)

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4
Q

what are the two basic circuits called in the basal ganglia?

A

direct and indirect (This is what allows the striatum to work on the GPi and SNR)

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5
Q

In general, the direct pathway of the basal ganglia is to? and the indirect pathway is to what?

A

direct pathway= bringing about wanted movements

indirect pathway= suppressing unwanted movements

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6
Q

Describe the pattern of the direct pathway of the basal ganglia?

A

1) striatum (caudate nucleus and putamen)
2) D1 receptors on MSN (substance P and dynorphin)
3) GPi/SNR
4) Thalamus
5) cerebral cortex
6) Motor action

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7
Q

which two areas have a major effect on the D1 and D2 receptors of the MSN’s?

A

Cortex (directly from brain)

SNC (releasing dopamine)

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8
Q

what are the differences between MSN’s that are activated by the D1 vs D2 receptors?

A

MSN’s start in the striatum and go to the GPi (direct) or to the GPe (indirect). Those going to the GPi contain substance P and dynorphin (D1 receptors), and those going to the GPe contain enkephalin (D2 receptors).

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9
Q

What activates the D1 and D2 receptors? where does this stuff come from?

A

1) dopamine

2) SNC

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10
Q

MSN’s projecting to the GPe are inhibitory/excitatory?

A

inhibitory. They prevent the inhibition of the of the STN by inhibiting the inhibitor.

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11
Q

what is the indirect pathway of the basal ganglia?

A

1) striatum
2) D2 receptor on MSN (enkephalin)
3) GPe
4) Subthalamic nuclei (STN)
5) GPi
6) Thalamus (VA)
7) Cerebral cortex
8) motor action

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12
Q

What is the key monoaminergic transmitter in basal ganglia function?

A

Dopamine

note that seratonin and norepinephrine also have a small affect

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13
Q

when mentioned in the notes as the striatum, what is generally being referred to?

A

putamen and caudate nucleus

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14
Q

what is the nigrostriatal pathway?

A

the pathway of dopamine release from the SNC to the caudate nuclei and putamen.

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15
Q

where do most axon terminals end of the dopaminergic axons coming from the SNC?

A

on the dendrites of the MSN in the striatum. (some end on interneurons)

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16
Q

T/F the globus pallidus, subthalmic nucleus, and SNR have dopamine input?

A

True (clarification needed here) page 3 basal ganglia 2

17
Q

dopamine released into the striatum promotes what?

A

movement!

18
Q

what does dopamine do to the D1 receptors? D2 receptors?

A

dopamine is excitatory to the D1 receptors, and inhibitory to the D2 receptors.

19
Q

If I have an idea to move, how do I get to the point where I release dopamine?

A

1) Idea in frontal cortex
2) striosomal pathway (striatum to SNC)
3) SNC to striatum through dopamine releasing neurons.
4) release of dopamine on MSN neurons in desired loop (direct and indirect)

20
Q

what is a hypokinetic disorder?

A

akinesia or the inability to move like normal

21
Q

Is Parkinsons disease hypo or hyper kinetic?

A

hypokinetic

22
Q

what causes parkinsons disease?

A

the loss of dopaminergic neurons in the SNC

23
Q

The loss of dopaminergic neurons releasing dopamine causes a decrease in dopamine being released in the striatum. What are the down stream affect of this on the direct pathway?

A

1) no dopamine=no activation of D1
2) no inhibition GPi/SNR
3) GPi/SNR can now inhibit thalamus.
4) No stimulation of cortex by thalamus

24
Q

what if you have a stroke that affects the basal ganglia? SNC?

A

This can cause parkinsons

25
Q

What drugs/chemicals can you use to treat parkinsons? Why can you use this?

A

L-dopa, because it undergoes a decarboxylation reaction to make dopamine.

26
Q

What is one of the major problems of using L dopa?

A

Its half life in the blood is very short so only very little actually is functional by the time it gets into the brain.

27
Q

What would a lesion in the GPi nucleus or neurons (pallidotomy) do for parkinsons?

A

stop the inhibition to the thalamus.

28
Q

Why is high frequency stimulation to the STN helpful in treating parkinsons?

A

it jams the signals traveling from the STN to the GPi/SNR. (Down-regulating the positive signal for thalamic inhibition from the GPi/SNR)

29
Q

What is Chorea?

A

sudden and involuntary movements of the body.

30
Q

Huntingtons disease is characterized by chorea. Why do the these patients who have a triple repeat sequence have this problem?

A

It affects the MSN neurons leading to the GPi/SNR and GPe

31
Q

Which MSN’s are most affected by Huntingtons disease? Which pathway does this affect?

A

The MSN’s containing enkephalin stemming. It affects the indirect pathway. This reduces inhibition to the thalamus causing Chorea.

32
Q

what is hemiballismus?

A

a disease that causes chorea because of a lesion in the STN.

33
Q

what is progressive supranuclear palsy?

A

degeneration of STN, SNR, and globus pallidus causing progressive palsy.