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Flashcards in Basal Ganglia Deck (23):
1

Describe the components of the Basal Ganglia.

striatum
globus pallidus (pallidum)
subthalamic nucleus
substantia nigra

2

What are the components of the striatum?

caudate nucleus and putamen
(nucleus accumbens)

3

What are the components of the globus pallidus (pallidum)? Describe its function in a broad sense.

Internal segment (GPi)
External segment (GPe)

GP is major efferent part of BG structure, information flowing into striatum, most info from cerebral cortex, chewed up analyzed then spit out to parts of globus pallidus which will either turn on or turn off parts of thalamus. normal setting is to turn thalamus off.

4

What are the components of the substantia nigra?

2 parts

compact part (SNc) - neurons that secrete dopamine
reticular part (SNr)- has function SIMILAR to globus pallidus internal (one of BG output nuclei)

5

Describe the subthalamic nucleus.

Part of BG, is located below thalamus.

receives input from cortex ("rapid access" to the BG or hyperdirect pathway) and GPe, output is excitatory to GPi and SNr neurons. Important for inhibiting unwanted movements

6

Describe GPi and reticular part of substantia nigra.

GPi - internal part of globus pallidus
reticular part of substantia nigra

both have similar functions, they are SEPARATE but their roles is SIMILAR (TRICKY on exam)

7

What name do globus pallidus and putamen together go by?

reticular nucleus

8

What does the anterior and posterior limbs of the internal capsule run through?

anterior limb of internal capsule between putamen and caudate

posterior limb of internal capsule separates globus pallidus and thalamus

(based upon image on slide 7)

9

Describe light/darker color on a myelin stain.

white matter will be dark and bunches of neurons appear lighter

10

Describe an overview of basal ganglia circuitry regarding the cortex, striatum, GPi/SNr and thalamus.

Cortex (gets input from frontal lobes) activates/excitatory effect on different parts of striatum

striatum has an inhibitory effect on GPi and SNr ...turns them off because they normally have an inhibitory effect on the thalamus

so thalamus is more active and communicating with cortex


Indirect: cortex to striatum to GPe to subthalamic nucleus to GPi and back to thalamus ("no go")

11

What is the lentiform nucleus?

segment including putamen, GPe and GPi
(see slide 13)

12

How does BG influence lower motor neurons?

BG has no NO MAJOR OUTPUTS to LMNs

influence LMNs via cerebral cortex

13

Describe the input to striatum. Name the neurotransmitter.

What is principal output from BG? Name neurotransmitter.

input to striatum from cortex is excitatory
glutatmate is the neurotransmitter

principle output from BG is via GPi and SNr
output is to thalamus then to cortex
GABA is neurotransmitter

(balance of excitatory and inhibitory inputs to striatum determine whether thalamus is suppressed)

14

Describe thalamocortical projections.

Excitatory
concerned with motor "intention"

15

Describe the BG circuits as parallel loops.

Motor loop (concerned with learned movements)
-direct pathway (five neuron pathway)
-indirect pathway (seven neuron pathway)

Cognitive loop (concerned with motor "intention")

Limbic loop (emotional aspects of movements)

Oculomotor loop (concerned with voluntary saccades- fast eye movements)

(different parts of the cortex feed into different parts of the striatum and have different effects)

16

Describe ventral striatum.

nucleus accumbens and adjacent putamen and caudate

(limbic inputs reach not only the nucleus accumbens, but adjoining parts of the putamen and caudate nucleus so, these limbic-recipient regions are recognized as a separate striatal division

(striatum and pallidum are somatotopically organized and permit selective inhibition of unwanted movements)

17

Describe ventral pallidum.

(part of GP)
small extension of the GPi under the anterior commissure

(striatum and pallidum are somatotopically organized and permit selective inhibition of unwanted movements)

18

Describe the motor circuit direct pathway in detail.
Involve association cortex, premotor cortex, substantia nigra, Caudate/putamen, VA/VL complex of thalamus, and GPi

See diagram on slide 19.

Association cortex turns on caudate/putamen (they turn off GPi) (group of neurons in striatum that contribute to direct pathway get excited from cortex and turn off GPi, so turn off inhibitory)

GPi then has less of an effect and the VA/VL complex of thalamus is more active and talking to premotor cortex

Substantia nigra also has a D1 receptor that makes caudate/putamen even more active and will inhibit GPi even more

1. Cortex excites striatum
2. Striatum inhibits GPi
3. thalamus is disinhibited
4. Cortical activity facilitated
(striatum inhibition on GPi is maximal, thalamic activity is increased, cortex is "excited" ...when striatum inhibition on GPi is minimal thalamic activity is decreased and cortex is "inhibited"

19

Describe the motor circuit indirect pathway in detail.

Association cortex has a excitatory effect on caudate/putamen... which will inhibit GPe (which inhibits subthalamic) so if GPe is inhibited then subthalamic nucleus is more active and will stimulate GPi and make it more inhibitory

GPI will then have a tonic, inhibitory affect on VA/VL complex of thalamus which goes to motor cortex

"no go"

D1 receptor from substantia nigra is excitatory and will increase the direct pathway going to GPi

D2 receptor from SN is inhibitory and will cause less inhibition of GPe and that means more inhibition of subthalamic nucleus so less actiation of GPi which allows for more "go" to thalamus and movement to occur...

with dopamine - movement
without dopamine - KEEP movement from occurring

20

Describe Parkinson's disease.

Not getting as much movement, someone moving slow, loss of spontaneous movement, hunched over, speech softer, problems with postural reflex

(lose dopamine input to brain) GPi becomes disinhibited and so it has MORE inhibition of thalamus

will see a loss of pigmented neurons on SN

21

Describe Huntington's disease.

autosomal dominant
chromosome 4 -Huntingtin gene
abnormal trinucleotide repeat expansion
onset age 30-50
initial symptoms chorea and alternation of mood
disease progression - dementia worsening, personality changes

see abnormal movement...the lateral ventricle normally indented by caudate nucleus (comma shape) then in H. you develop degeneration in striatum and in caudate nucleus so ventricle takes on oval shape

problem is degeneration in caudate/putamen (effect is opposite of Parkinson's) so GPi is turned off and there is numerous spontaneous movements and difficulty with control...hypermovement disorder

due primarily to a loss of cholinergic and GABAergic neurons in the striatum. Thought to be associated with glutamate-induced toxicity and cell death.

22

Parkinson's is an example of a deficit due to loss of a specific neurotransmitter (dopamine). What do lesions and diseases affecting other areas of the BG system typically result in?

result in involuntary movements:

tremors -rhythmic oscillatons
athetosis- slow, writing (snake like) movements
chorea- abrupt movements of limbs and face "tics"
ballism- violent, flailing movements
dystonia - distorted body positions and posture

most of these symptoms are due to the release of normally inhibited patterns.

23

What is Hemiballismus?

due to loss of ONE of the subthalamic nuclei, usually due to a cerebral vascular accident (stroke) or tumor. Characterized by ballistic movements restricted to one side of the body.