Abstract
The administration of carbidopa (5–50 mg/kg), peripheral L-aromatic aromatic aminoacid decarboxylase inhibitor, significantly increased striatal tyramines; maximal effects were observed at 2–4 hr after treatment. Benserazide produced similar effects. The drug, NSD 1034, that inhibits both central and peripheral decarboxylase, produced a dose-dependent reduction in striatal p-tyramine; in contrast, concentrations o of m-tyramine were increased by the smaller doses (2–20 mg/kg) and reduced by the larger dose (400 mg/kg). The results support the view that the tyramines are formed within the brain by decarboxylation of their parent aminoacids but by different mechanisms.
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