Abstract
Abstract— In rabbits, the sedative effect of chlorpromazine (CPZ) is temporally correlated with a decrease in dopamine and a rise in homovanillic acid (HVA) in the basal ganglia. Reserpine elicits similar biochemical changes. In addition, both reserpine and CPZ reduce the concentration of 3‐methoxytyramine, the O‐methylated metabolite of dopamine in the basal ganglia of normal rabbits. In contrast, both drugs markedly increase the levels of this metabolite in animals treated with a monpamine oxidase inhibitor. The results indicate that CPZ, like reserpine, causes an intraneuronal destruction of dopamine, and suggest that the well‐documented increase in dopamine synthesis after CPZ is the consequence of this mechanism and not of a blockade by CPZ of the dopaminergic receptors in brain.
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