All about the ganglia (basal, that is) Flashcards

1
Q

Input areas of the basal ganglia (who receives input?)

Input comes from the __ or the __

A

Input areas of the basal ganglia are the caudate nucleus and the putamen

Input comes from the cortex or from the thalamus

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2
Q

Output areas of the basal ganglia (i.e. path of signal from input areas)

A

After processing of input, the output leaves from the globus pallidus internal or it goes to the pars reticularis of the substantia nigra

That goes back up to the thalamus and then to the cortex

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3
Q

Direct vs indirect pathway of BG circuit

A

Information processed from putamen or caudate nucleus can either go directly into the globus pallidus internal then to the thalamus (see previous slide); DIRECT pathway

OR

It can go into the globus pallidus internal, then to the subthalamic nucleus then to the globus pallidus external, then back to the globus pallidus internal then to the thalamus/cortex; INDIRECT pathway

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4
Q

___ ___ of the substantia nigra – contains dopaminergic neurons that innervate the __ nucleus and the ___; loss of these = Parkinson’s disease.

The subthalamic nucleus also receives direct excitatory input from the ___

A

Pars compacta

Caudate nucleus and putamen

Cortex

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5
Q

Parallel processing loops (hint: LMAO!!)

location of each loop (e.g. for motor - premotor and supplementary motor areas)

A

Motor (premotor, supplementary motor area)

Occulomotor (frontal eye field, saccades)

Association (prefrontal cortex)

Limbic (cingulate gyrus)

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6
Q

Cells in the caudate nucleus and putamen (what are they called, what do they do? there’s 2 populations; hint: something about spines)

A

Within the caudate nucleus and the putamen, most of the neurons are Medium spiny neurons (aka GABAergic/inhibitory projection neurons); they start from the caudate/putamen and project long distances

The other neurons are aspiny neurons: interneurons; can be cholinergic or send other signals; their modulatory role is not well understood

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7
Q

The cells in the globus pallidus internal and the substantia nigra reticularis

A

GABAergic projection neurons similar to those in caudate nucleus and putamen

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8
Q

At baseline:

The cells in the CN and P are firing at a very ___ rate, while those in the GP and SN are firing at a ___ rate

After processing of input:

As signal leaves input area, it leaves at ___ activity, then as it leaves from the output areas, it leaves at ___ activity

A

low

high

high

low

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9
Q

Cortical input is ___

So cortical input acting on the GABAergic neurons is going to ___ their INHIBITORY activity on the output neurons, so the output is (more/less)___ inhibitory, and the final effect going from the thalamus back to the cortex is ___

A

Cortical input is stimulatory

So cortical input acting on the GABAergic neurons is going to INCREASE their INHIBITORY activity on the output neurons, so the output is LESS inhibitory, and the final effect is disinhibition (i.e. the signal that’s sent to the cortex is a stimulatory signal because the inhibition on the thalamus has been removed)

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10
Q

Indirect pathway:

Input comes from cortex (stimulatory) and acts on the GABAergic neurons in the CN/P. From there, an increasingly ___ signal is sent to the GABAergic neurons in the globus pallidus external, which ___ inhibition to the neurons in the subthalamic nucleus, so the signal from there is ___. That then ___ the inhibitory signal to the thalamus, and from there to the cortex, the signal is ___

(essentially, using the indirect pathway results in more ___)

A

Input comes from cortex (stimulatory) and acts on the GABAergic neurons in the CN/P. From there, an increasingly inhibitory signal is sent to the GABAergic neurons in the globus pallidus external, which decreases inhibition to the neurons in the subthalamic nucleus, so the signal from there is stimulatory. That then increases the inhibitory signal to the thalamus, and from there to the cortex, the signal is inhibitory

(essentially, using the indirect pathway results in more inhibition, NOT DISINHIBITION)

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11
Q

Role of basal ganglia in gating motor activity:

T/F: disinhibition of thalamocortical pathway by the BG cause motor activity

T/F: The disinhibitory signal from the BG to the thalamocortical pathway tells the motor system which neurons should discharge, as well as how strongly they should discharge.

A

Disinhibition (direct pathway) by basal ganglia basically brings us closer to motor activity but doesn’t actually cause motor activity (indirect pathway has opposite effects)

Basal ganglia also enable certain movements and control their sequence but they don’t cause them (so basically the signal from the cortex is the cause of things, the BG are just middle men)

The disinhibitory signal from the BG to the thalamo-cortical pathway tells the motor system which neurons should discharge rather than how strongly they should discharge.

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12
Q

Function of indirect pathway:

(why is it contrast-enhancing, what else does it do?)

A

The indirect pathway is contrast-enhancing in that all other pathways surrounding the direct pathway are shutdown so that the cortex knows to receive signals only pathway? (I think)

The indirect pathway also dampens the activity in the direct pathway

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13
Q

Role of dopamine in indirect vs direct pathway:

dopamine will always cause an ___in activity, regardless of which path its acting on

The Dopaminergic neurons in the indirect pathway in the CN and P are inhibitory; they express the __receptor, which when activated is inhibitory

The dopaminergic neurons in the direct pathway are ___ b/c they express the D1 receptor which when activated is excitatory

A

The Dopaminergic neurons in the indirect pathway in the CN and P are inhibitory; they express the D2 receptor, which when activated is inhibitory

The dopaminergic neurons in the direct pathway are excitatory b/c they express the D1 receptor which when activated is excitatory

(dopamine will always cause an increase in activity, regardless of which path its acting on)

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14
Q

Role of glutamate in direct vs indirect pathway

A

Glutamate does the opposite; in the direct pathway, it causes stimulation but in the indirect pathway it causes a decrease in stimulation/inhibition

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15
Q

The neurons of the globus pallidus are involved in ___

A

Postural adjustments

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16
Q

Ballismus (recall the indirect pathway involving the glutaminergic neurons)

Happens as a result of damage to the __

Characterized by __ __ movements of one limb

T/F: Ballismus is usually unilateral

A

subthalamic nucleus (specifically, the Glutaminergic neurons in the STN are dead/destroyed),

which results in an abnormal increased activity/signal to the cortex

uncontrolled flinging movements of one limb

Truth. Ballismus is usually unilateral.

The increased signal pushes the drive closer to the threshold for firing of the motor neurons, such that your limbs will jerk/move when you have no intention for them to do so

17
Q

Parkinson’s disease:

cause

what’s the final signal that’s sent to the cortex (hint: this explains some of the symptoms, e.g. freezing) why is this the case?

A

Caused by loss of dopaminergic neurons in the pas compacta of the substantia nigra

Final signal to the cortex is inhibitory, which pulls the thalamocortical drive further away from initiating a movement (that would explain some of the symptoms, e.g. freezing)

18
Q

Huntington’s disease

cause

net effect on cortex

symptoms

A

caused by loss of medium spiny neurons in the caudate nucleus and the putamen (the GABAergic guys) in the indirect pathway

net effect of loss of GABAergic neurons in the caudate nucleus and putamen is increased activity going to the cortex (hence the uncontrolled movements because the drive for neuron firing is now set closer to threshold)

generalized uncontrolled movement; increased ballistic movements

19
Q

Treatment of Parkinson’s disease vs Huntington’s disease

which version of the treatment of Parkinson’s do you give and why?

what happens when you increase the dose of this treatment?

What is the side effect of using the Huntington’s treatment?

A

L-Dopa gets converted to dopamine peripherally by the few neurons that are still alive. Eventually, the pt loses too many neurons and infusing L-dopa won’t make much of a difference because they won’t have enough enzyme left to convert L-Dopa to Dopa anyway

When you increase the L-Dopa concentration as the disease progresses, the pt starts to develop Huntingon’s like symptoms (tardive dyskinesias)

Using dopamine receptor blockers (either for some psychiatric conditions or for Huntington’s disease) can result in Parkinson’s like symptoms

Using dopamine receptor blockers (either for some psychiatric conditions or for Huntington’s disease) can result in Parkinson’s like symptoms

20
Q

Treatments for Parkinson’s disease

A

Embryonic nigral stem cells

Trophic factors (GDNF)

Targeted surgical ablation of STN or GPi

DBS high frequency stimulation of STN

21
Q

Function of GDNF in treating Parkinson’s disease

Difference in effect of GDNF in substantia nigra vs neostriatum

A

GDNF: one of the trophic factors that is neuroprotective of dopaminergic neurons

GDNF: not significantly neuroprotective when placed in the substantia nigra (actually caused some weird structural changes)

GDNF: significantly neuroprotective when placed in the caudate and the putamen (aka the neostriatum)

22
Q

Role of deep brain stimulation in Parkinson’s disease:

what is it/how do you do it?

what’s the net effect?

A

Deep brain stimulation: basically you pass an electric current through the STN which apparently relieves symptoms in patients with Parkinson’s disease

**the probe is an electrode as well as a cryoprobe**

Deep brain stimulation somehow enhances the effects of the neurons in the STN and the GP, so the net effect of DBS is increased activity to the cortex

23
Q

Define optogenetics

function of channelrhodhopsin

halorhodopsin

A

Optogenetics: basically you add exogenous molecules into the membranes of cells (neurons) with the goal of excitation or inhibition

Channelrhodhopsin: excitatory – activated by light only (blue light); causes membrane depolarization when activated (brings Na in and kicks K+ out of the cell)

Halorhodopsin: inhibitory – activated by (yellow) light; (brings Cl- into the cell); causes membrane hyperpolarization

24
Q

difference between deep brain stimulation and optogenetics (who’s more specific?)

A

With deep brain stimulation, you don’t know which neurons you’re actually activating because you’re stimulating everything in the general area

With optogenetics, you can target specific neurons