Abstract
Early in the 1960’s, it became apparent that the known ability of α-methyl aromatic amino acids to inhibit aromatic amino acid decarboxylation (Sourkes, 1954; Westerman, Balzer, and Knell, 1958; Denglerand Reichel, 1958; Smith, 1960) was not solely responsible for the depression of biogenic amine concentrations in tissues following the administration of α-methyldopa or α-methyl-m-tyrosine to animals. Norepinephrine concentrations in the tissues of animals which received the amino acids returned to normal considerably more slowly than serotonin and dopamine concentrations (Hess et al., 1961; Porteret al., 1961; Stone et al., 1961), and considerably more potent decarboxylation inhibitors had little effect upon tissue catecholamine concentrations (Udenfriend and Zaltzman-Nlrenberg, 1962).
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