The Ca++-antagonist nimodipine decreases and the Ca++-agonist Bay K 8644 increases catecholamine synthesis in mouse brain.
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.
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology*; D006916:5-Hydroxytryptophan / Q000096:biosynthesis; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002395:Catecholamines / Q000096:biosynthesis*; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism; D004295:Dihydroxyphenylalanine / Q000096:biosynthesis; D007473:Ion Channels / Q000187:drug effects; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D009553:Nimodipine / Q000494:pharmacology*
D002395:Catecholamines; D007473:Ion Channels; D009553:Nimodipine; D004295:Dihydroxyphenylalanine; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D006916:5-Hydroxytryptophan