The first demonstration of an animal model for PD was reported by Carlsson in the 1950s using rabbits treated with reserpine. Reserpine is a catecholamine-depleting agent that blocks vesicular storage of monoamines. The akinetic state, resulting from reserpine-induced dopamine depletion in the caudate nucleus and putamen, led Carlsson to speculate that PD was due to loss of dopamine neurotransmission. This speculation was supported by the discovery of reduced striatal dopamine in postmortem brain tissue of PD patients and led to the subsequent use of levodopa (in conjunction with a peripheral dopa-decarboxylase inhibitor) for symptomatic treatment of PD (2,3). Thus, the initial observations derived from an animal model led to an important clinical therapy that still remains the "gold standard."
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