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Ultrastructural immunocytochemical Synapse Changes In A Rat Model Of Parkinson’s Disease
Published online by Cambridge University Press: 02 July 2020
Extract
Parkinson's disease is a progressive disorder that is characterized by degeneration of the dopamine containing neurons located within the midbrain (substantia nigra). There is also substantial loss of dopamine within nerve terminals located within the striatum which originate from those dopamine neurons. Current therapy involves administration of the precursor to dopamine, namely l-dopa. This chemical is taken up into the brain and then converted to dopamine. Although replacement of dopamine is effective over the first few years, other movement disorders are associated with longterm l-dopa therapy. The l-dopa induced dyskinesias limit the usefulness of this type of therapy.
Although loss of dopamine is the major neurochemical deficit in Parkinson's disease, other neurotransmitters within the striatum may also be altered. There is a major axonal projection from the cortex to the striatum. The corticostriatal pathway uses the excitatory neurotransmitter, glutamate, and dopamine is known to modulate the activity of glutamatergic synapses
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