Parkinson’s Disease And Action Of Drugs On Movement

728 words - 3 pages

Parkinson’s Disease and Action of Drugs on Movement

Introduction:

Parkinson’s disease is a neurological disorder that seriously impairs
motor function, with people afflicted with this condition exhibiting
akinesia, muscle rigidity and having a tremor at rest. It is accepted
that the loss of motor function is brought upon by the progressive
degeneration of nigrostriatal dopamine neurons, which leads to a
corresponding loss of dopamine in the caudate/putamen part of the
basal ganglia, which is accepted as the main receiving area in motor
circuits. Information coming to it from the cortex and thalamus is
processed and channeled to the pallidum and to the substantia nigra
reticular. There are two main pathways from the striatum to the
pallidum, the direct pathway and the indirect pathway, and so loss of
dopamine, which usually serves to activate the direct pathway and
inhibit the indirect pathway, results in a loss of the tonic
inhibitory influence on GABA output pathways from the striatum. This
accounts for the resulting loss of motor control.

Dopamine is a catelcholamine and acts as a neurotransmitter activating
dopamine receptors of which five types exist with D1 and D2
predominating. Aside from functioning as a neurotransmitter, dopamine
is also the precursor to noradrenaline in all central and peripheral
noradrenergic neurons. Dopamine is made from the precursor Tyrosine
which is converted to DOPA by the enzyme tyrosine hydroxylase, and
DOPA is then converted to dopamine by the enzyme dopa decarboxylase.
This enzyme has a much higher activity in comparison to tyrosine
hydroxylase so under normal conditions there is little or no
endogenous DOPA found in most cells.

The first line of treatment for a patient is to replenish their
dopamine stores, which have diminished due to loss of dopaminergic
neurones. As dopamine cannot cross the blood-brain barrier it is of no
use to simply administer dopamine, instead its precursor L-DOPA is
given. This...

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