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Basal ganglia


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How is the basal ganglia involved in motor function?
It modulates motor output: in essence it decides which movement will be performed given a range of stimuli.
What five structures make up the basal ganglia?
3.Globus pallidus
5.Substantia nigra
Other than motor signals from the cortex, what are three kinds of information the basal ganglia receives?
1.Sensory information
2.Motivational state
3.Emotional state
What are the major outputs from the globus pallidus? What neurotransmitter dominates these pathways?
*to the thalamus and subthalamus
What are the major outputs from the caudate and putamen? What neurotransmitter dominates these pathways?
*to the globus pallidus and substantia nigra
What are the major inputs to the caudate and putamen? What neurotransmitters dominate these pathways?
*from the cerebral cortex and substantia nigra to the caudate and putamen
*from the substantia nigra - dopamine
*from the cortex - glutamate
What three neurotransmitters dominate basal ganglia circuits? Are they inhibitory or excitatory?
1.GABA - inhibitory
2.Dopamine - excitatory
3.Glutamate - excitatory
How is output from the basal ganglia similar to output from the cerebellar cortex?
They both are all inhibitory
Name the 4 dyskinesias seen with damage to the basal ganglia.
2.Resting tremor
What is the incidence of PD in the general population? In adults over age 70? What percentage of PD patients are under age 50?
Are men and women equally affected by PD?
No - men are twice as likely to have PD than women.
Give 4 of the characteristic symptoms of PD.
2.Resting tremor
5.Characteristic gait - short steps, stooped posture, little arm movement
What neurons degenerate in PD?
The dopaminergic neurons of the substantia nigra.
What is the cause of the majority of PD cases? Name some environmental factors postulated to be at play. With what lifestyle has PD been associated?
*most cases have an idiopathic etiology
*exposure to carbon monoxide, carbon disulfide, cyanide, manganese
*farming and well water
Two classes of medication are used to alleviate the symptoms of PD. What are these and what symptoms does each alleviate?
1.Dopaminergic agonists - alleviate bradykinesia, slow gait, rigidity
2.Cholinergic antagonists - alleviate resting tremor
Why is the effectiveness of medication limited in PD patients?
Patients develop tolerance and require larger and larger doses. Eventually the size of the dose eclipses the margin of safety. Also there are significant side effects associated with these drugs.
Name two surgical techniques aimed at alleviating the symptoms of PD.
1.Specific lesioning of the globus pallidus (pallidotomy)
2.Transplant of fetal or stem cell dopaminergic neurons.
MPTP has been shown to destroy dopaminergic neurons in the substantia nigra and cause a syndrome almost identical to PD. In what way is this condition different from PD?
Rather than the gradual onset seen in PD patients, individuals who have been administered MPTP show sudden destruction of neurons and dramatic onset of symptoms.
Typically, what are the first signs of HD? How does this frequently lead to misdiagnosis?
*emotional lability and disorders in mood
*often misdiagnosed as a psychiatric illness
What are the motor symptoms of HD? How do these symptoms contribute to the death of these patients?
*progressive inability to walk, speak, and swallow
*bacterial pneumonia secondary to aspiration
What is the incidence of HD? Are men and women equally affected?
*men are twice as likely to have HD than women
What is "anticipation" as seen in HD? How was this phenomenon explained biochemically?
*age of onset decreases and severity of symptoms increases with successive generations
*the number of CAG triplet repeats increases with successive generations
Though HD patients eventually show widespread degeneration of brain tissue, where does this pathology generally begin?
With destruction of GABA-nergic (medium spiny neurons) in the caudate and putamen.
Is the genetic mutation that causes HD recessive or dominant? How is this mutation expressed in the affected genome?
*autosomal dominant
*expansion of CAG triplet repeats in the huntingtin gene from 10-35 to 40-100
It is known that the genetic mutation in HD causes an accumulation of an insoluble polyprotein, but why does this fail to explain the pathology seen in the disease?
The effects of polyglutamine on neurons is not known. Also, this gene is expressed throughout the body but only the GABA-nergic neurons in the caudate and putamen are affected.

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