Abstract
The effects of the Ca ++-antagonist nimodipine and the Ca ++-agonist Bay K 8644 on brain catecholamine synthesis in male albino mice were investigated in vivo. Nimodipine caused a dose-dependent reduction in the synthesis rate of dopamine and noradrenaline, measured as the accumulation of 3,4-dihydroxyphenylalanine (DOPA) after inhibition of the L-aromatic amino acid decarboxylase with 3-hydroxybenzylhydrazine (NSD 1015). In contrast, Bay K 8644 caused an increase in DOPA synthesis. Furthermore, Bay K 8644 dose-dependently antagonized the effect of nimodipine. It is suggested that nimodipine and Bay K 8644 induced these changes by interfering with neuronal Ca ++ transport, thus arguing for a role of voltage operated Ca ++ channels in normal nerve function.
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