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Flashcards in basal ganglia Deck (35)
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1

1. Give a general description of the role of the basal ganglia in motor control.

Modulation of motor performance by massive interconnections with motor cortices

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2. What is the major source of input to the basal ganglia? And which are the input/output nuclei

cerebral cortex. The caudate and putamen are input nuclei b/c they are closest to the cortex. Info flows from caudate and putamen to globus pallidus, then to the thalamus and back to cortex, so globus pallidus is major output nucleus

3

why are basal ganglia most susceptible to metabolic disruption

Basal ganglia are enriched in neurotransmitter biosynthesis (ie 80% of dopamine in the brain is here)

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3. Describe the character and probable cause of Parkinson's disease.

Difficulty in initiating movement or performing sequential complex movements. Caused by degeneration of substantia nigra neurons and loss of dopamingergic input

5

List the nuclei of the basal ganglia

caudate and putamen (collectively called neostriatum), globus pallidus (external and internal portions), substantia nigra and subthalamic

6

Principal output nucleus of basal ganglia

Internal portion of globus pallidus

7

Do basal ganglia control ipsilateral or contralateral body

Because the basal ganglia on one side interact with the cortex on that same side, unilateral defects in the basal ganglia are seen as contralateral deficits in function. That is, the left basal ganglia control movements of the right side of the body (in contrast to the cerebellum).

8

List function of the basal ganglia nuclei

neostriatum: inputs from cortex. Globus pallidus: outputs to thalamus. Substantia nigra: internal feedback loops. Receives projections from striatum and projects back to striatum or to the thalamus. Subthalamic: receives projection from external segment of globus pallidus and projects back to external and internal globus pallidus (pallidal feedback loop)

9

Which specific part of cortex projects to the Putamen and where do fibers go from putamen

Sensori-motor cortex projects to putamen. Putamen in turn projects to its own subsection of globus pallidus, which in turn projects mostly to VA (some VL) thalamus. These thalamic nuclei in turn project back to motor cortex, especially supplementary motor area (SMA)

10

Which specific part of cortex projects to the caudate and where do fibers go from there

The caudate receives input widely from frontal association cortex (the frontal lobes), sends its information to its own region of globus pallidus, and from there to dorsomedial thalamus, which in turn projects widely to association cortex

11

What is the nucleus accumbens and what is its function

Caudal juncture btw caudate and putamen. it processes information from paleo-cortex (near olfactory cortex) as part of the limbic system and subserves emotional and drive related aspects of behavior

12

which basal ganglia has a somatotopic map

putamen

13

4. Is the output of the basal ganglia inhibitory or excitatory?

Output of basal ganglia are Inhibitory!!!

14

Describe the direct pathway from cortex to basal ganglia

1. Cells in layer V of cerebral cortex (output cells) send axons to synapse in basal ganglia where they release glutamate to excite cells in caudate or putamen. 2. Cells in caudate or putamen send axons to globus pallidus where they release GABA to inhibit cells there. 3. The cells in globus pallidus send axons to thalamus where they release GABA to inhibit
cells there. 4. Thalamic neurons can then excite cells in cortex1. Cells in layer V of cerebral cortex (output cells) send axons to synapse in basal ganglia where they release glutamate to excite cells in caudate or putamen. 2. Cells in caudate or putamen send axons to globus pallidus where they release GABA to inhibit cells there. 3. The cells in globus pallidus send axons to thalamus where they release GABA to inhibit
cells there. 4. Thalamic neurons can then excite cells in cortex1. Cells in layer V of cerebral cortex (output cells) send axons to synapse in basal ganglia where they release glutamate to excite cells in caudate or putamen. 2. Cells in caudate or putamen send axons to globus pallidus where they release GABA to inhibit cells there. 3. The cells in globus pallidus send axons to thalamus where they release GABA to inhibit
cells there. 4. Thalamic neurons can then excite cells in cortex

15

Basal firing rate of basal ganglia

Globus pallidus neurons fire spontaneously at high rates, while striatal neurons fire very slowly. In absence of cortical input, globus pallidus inhibits thalamo-cortical input. A signal will excite striatal neurons causeing inhibition of pallidus and disinhibiting thalamo cortical pathway. This leads to positive feedback to cortex

16

Describe pathway of substantia nigra activation

Striatal neurons release GABA to inhibit substantia nigra. When substantia nigra is not inhibited, it sends dopaminergic axons back to the striatum where dopamine is excitatory. Dopamine is released diffusely, perhaps humorally, into striatum. DA is excitatory to GABA-ergic output neurons but may be inhibitory to cholinergic interneurons in the striatum

17

D1/direct pathway

excitatory pathway: cortex releases glutamate and excites medium spiny neurons in caudate and putamen > striatum release GABA and inhibit globus pallidus internal > Gpi does not release GABA at thalamus thus thalamus is excited > thalamus excites cells in cortex

18

dopamines and acetylcholines effect on D1 pathway

dopamine is excitatory to striatum, so overall it will lead to excitation of cortex via D1 pathway. Acetylcholine has opposite effect

19

Pathway of subthalamic nucleus activation

The subthalamic nucleus receives an inhibitory input from external (lateral) globus pallidus and projects excitation back to the internal (medial) segment of globus pallidus. The functional consequence of a blow-out ("vascular accident") of the subthalamic nucleus is equivalent to disinhibition of thalamus, that is, loss of excitation to inhibitory neurons of globus pallidus

20

D2/indirect pathway

inhibitory pathway: cortex releases glutamate and excites medium spiny neurons in striata > striata release GABA and inhibit globus pallidus external > Gpe inhibits subthalamic nucleus > STN excites internal globus pallidus > Gpi releases GABA at thalamus and inhibits it > no excitation of corte

21

dopamine and acetylcholines effect on D2 pathway

dopamine is excitatory to striatum, so overall it will lead to inhibition of cortex via D2 pathway. Acetylcholine has opposite effect

22

Which disorders of basal ganglia are due to direct vs indirect pathway involvement

Hypokinetic disorders are due to decrease in direct pathway. Hyperkinetic disorders are due to decrease in indirect pathway

23

Describe the physical characteristics of Parkinsons

resting tremor- stops during intended movement. Increased tone due to activation of flexors and extensors simulataneously, difficulty in initiating movements, slowness of movement

24

Describe the brain structures affected by Parkinsons

Loss of dopamine neurons on substantia nigra. Since dopamine is excitatory to striatal neurons, this reduces disinhibition that striatum would produce in thalamus by way of globus pallidus.

25

Drug with Parkinsonian like effects

MPTP- causes death of dopaminergic cells in substantia nigra

26

Parkinsons treatment

L-dopa (ingested, crosses BBB), carbidopa (blocks degradation of dopamine), brain transplants (inject catecholaminergic tissue from brains of aborted fetuses into patients basal ganglia), deep brain stimulation

27

How does deep brain stimulation work

electrodes implanted in subthalamic neucleus or internal globus pallidus to stimulate neurons. Used for patients who still benefit from meds, but are disable by fluctuations btw on and off med states, or by med induced dyskinesias.

28

Chorea

Nearly continuous rapid movements of face, tongue or lips

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Athetosis

slow, writhing, ceaseless movements of hand, sometimes lips, tongue, neck and foot

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symptoms of Huntingtons

chorea or athetosis. Initially, relative hypokinesia or immobility, degradation of mood, loss of computational and memory skills

31

5. What is the genetic cause of Huntington’s Disease

Autosomal dominant- triplet repeat of CAG in the Huntingoton gene on Short arm of 4th chromosome. This codes for polyglutamine. 17-34 repeats is normal, >40 causes Huntingtons

32

What areas of the basal ganglia are affected in Huntingtons

Cholinergic striatal neurons and GABAergic medium spiny output neurons of striatum degenerate, possibly due to glutamate excitotoxicity. Loss of striatal actions on globus pallidus seem to cause dz symptoms. Too much exogenous dopamine can also produce symptoms

33

Dopamine axis in basal ganglia

Too little dopamine produces lack of movement (Parkinsonism), too much dopamine produces hyperkinesia (Huntington's chorea) (leading to the analogy that dopamine acts as "brain grease").

34

Hemiballismus- what is it, what causes it

Flailing movements of th arm and leg on one side. This results when a stroke in a small ganglionic branch of the posterior cerebral artery leads to damage of the subthalamic nucleus on one side (usually in the elderly). Loss of excitation by the subthalamic nucleus reduces inhibitory outflow of globus pallidus so motor programs are inappropriately initiated through the disinhibited thalamus.

35

What type of stimulus (depolarizing or hyperpolarizing) would you predict would be used for the “deep stimulation” treatment of Parkinson patients?

not sure yet