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12 Cards in this Set

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Diseases of basal ganglia result in what?
1. Hypokinetic Disorders (eg., Parkinson’s disease)
bradykinesia (akinesia)

2. Hyperkinetic Disorders (eg., Huntington’s chorea)
dyskinesia (dystonia)

In general the disorders can be described as Movement pop ups and disturb what you are doing at the present moment
Portion of basal ganglia circuits have gone bad.

Basal ganglia has parallel circuits that are antagonistic to each other.
What are the 4 functional definition of the basal ganglia?
1. Striatum or (Neostriatum)
a. caudate nucleus
b. putamen

2. Globus Pallidus (or Paleostriatum)
a. internal segment
b. external segment

3. Substantia Nigra
a. pars compacta: cell dense and has dopamine
b. pars reticulata: cell sparse and it has GABA

4. Subthalamus


The cerebral peduncle is made up substantia nigra and crus cerebri.
Illustrate the inputs and outputs of the functional basal ganglia in the direct pathway?
Inputs and outputs of the (functional) basal ganglia are processed by different nuclei:

1. caudate nucleus
2. putamen

1. globus pallidus, internal segment
2. substantia nigra, pars reticulata
1. Describe the evolvement of the internal capsule?

2. Describe the mosaic organization of the striatum?
1. Rodents lack an internal capsule, therefore, the putamen & caudate are a singular structure: the (neo)striatum
In mammals with an internal capsule, the caudate and putamen still fuse, rostrally.
Therefore, As the brain evolved, the internal capsule divided the caudate and their putamen and they fuse in the rostral end

A. What are the 3 areas that the Striatum receives its input from?

B. What are the 3 areas that the putamen receive its inputs from?

C. What are the 2 areas that the caudate nucleus receives inputs from?
A. The striatum receives inputs from:

1. (essentially) all areas of cortex
a. glutaminergic
b. excitatory

2. substantia nigra
a. pars compacta
b. dopaminergic

3. thalamus, intralaminar nuclei

B. The putamen received inputs from:
a. motor cortex
b. premotor cortex
c. somatosensory cortex

C. The caudate nucleus receives inputs from:
a. associational cortex
b. frontal eye fields


The putamen is the motor ending of the striatum.
B. P = PMS
C. C = CAF

1. Neurons of the striatum

2. Neurons of the globus pallidus and substantia nigra, pars reticularis

Describe the striatal ouput and what are the 2 ouput nuclei?
Striatal output is inhibitory and the 2 ouput nuclei are:

1. to the internal segment of the globus pallidus
2. to the pars reticulata of the substantia nigra
Describe the process of disinhibition of thalamic cells?
Excitatory cortical input into the striatum
results in disinhibition of thalamic cells.

normally striatial neurons are quiet & pallidal neurons have a high rate of spontaneous activity.
a pulse of corticostriatal input results in:
1. striatal excitation
2. pallidal inhibition
3. thalamic disinhibition

Therefore, you are going from a normally quiet striatal neuron with low firing frequency to a higher frequency firind due to the input from the cortex and this high striatal frequency will shut off the globus pallidus (pallidal inhibition) and the globus pallidus can no longer carry on its normal function of inhibitinh the thalamus so you know get thalamic disinhibition.
What is structurally evident in a brain affected by huntington's disease and why is this?
In Huntington’s disease, the striatum, specifically the caudate nucleus degenerates as evident by enlargement of the lateral ventricle. There is severe degeneration of the GABA - ergic neurons located in the caudate nucleus and putamen.
This disease causes chorea, a dance like gait.
What structure in the basal ganglia causes hemibalism and what are the connections of this structure?
Vascular lesions of the subthalamus are thought to produce hemiballism. The subthalamus is part of an indirect pathway through the basal ganglia.
1. What is evident in a brain affected by Parkinsons?

2. Illustrate why the area of the brain affected by parkinson's is important to the striatum?
1. Lesion of the substantia nigra (SN), pars compacta, and depletion of striatal dopamine are consistently found in the brains of Parkinsonians

2. Dopamine from the substantia nigra pars compacta (SNc) modulates the neural activity in the striatum.

Lesion of SNc results in Parkinson’s Disease
A. What are the 3 major symptoms of parkinson's disease?

B. What are the 4 basic strategies for treating parkinson's disease?
A. The 3 major symptoms of Parkinson’s disease:

1. resting tremor
2. rigidity
3. bradikinesia - can lead to akinesia (no movement).

B. The 4 basic strategies to treat Parkinson's are:

1. L-dopa (replacement) therapy (dopa is used instead of dopamine because it can cross the blood brain barrier but dopamine cannot)

2. stereotaxic lesions of the internal segment of the globus pallidus (GPi, pallidotomy)

3. deep brain stimulation of GPi or subthalamus (in clinical trial stage)(electrodes into the brain)

4. brain transplant (no comment)


1. L-Dopa Therapy: treating the symptoms -

-it is the gold standard
-it does not stop the disease process
-it is not, therefore, an effective strategy in more advanced stages of Parkinson’s disease (when too few cells are remaining)
-it does not exposed the brain to a continuous dose of dopamine when administered in oral doses
-it produces, therefore, on/off side effects (often chorea)

2. Stereotaxic Surgery
Using stereotaxic coordinates, an electrode can be position in the globus pallidus which then can be electrolytically lesioned.

3. Disadvantages of Electrolytic Lesions

-difficulty in placing the electrode in the precise location for lesion due to variability in brain size
-difficulty in determining and controlling the optimal size of the lesion
-impossibility of adjusting the lesion size based on the patient’s response
-complication from unexpected hemorrhage and/or infection due to rupture of blood vessels

4. Deep Brain Stimulation
currently is being tested in clinical trials
avoids many of the limitations of lesion
most importantly, stimulation strength can be constantly adjusted to optimize therapeutic action as the disease progresses; so basically you place electrode in diseased part of the brain, implant it, and stimulate at high frequency.


Over 100 neuroactive substances have been identified in the striatum