Effect of acute ethanol treatment on transmitter synthesis and metabolism in central dopaminergic neurons
Bustos, G.; Roth, R.H.
Journal of Pharmacy and Pharmacology 28(7): 580-582
1976
ISSN/ISBN: 0022-3573 PMID: 8613 Document Number: 102580
Ethanol given to rats enhanced the synthesis of brain catecholamine, particularly dopamine, measured as dopa accumulation after inhibition of aromatic amino acid decarboxylase (Carlsson and Lindqvist, 1973). Waldeck (1974) reported that ethanol administered to mice had no effect on catecholamine synthesis as measured by the accumulation of dopa following inhibition of the decarboxylase. The discrepancy between these results led to this study of the effect of acute ethanol treatment upon dopamine synthesis in rat neostriatum. Ethanol, 20% (wt/vol), and the amino decarboxylase inhibitor Ro-4-4602 (seryltrihydroxy-benzylhydrazine) were administered i.p. to rats. To determine the effect of ethanol treatment on dopamine synthesis, the accumulation of dopa after inhibition of dopa decarboxylase was followed and an approximation of the rate of dopamine synthesis was obtained. The technique also provided an in vivo estimate of tyrosine hydroxylase activity. Ethanol treatment had no effect on dopamine synthesis. An increase in dihydroxyphenylacetic acid accumulation was noted after ethanol administration, possibly mediated via an increase in impulse flow in dopaminergic neurons. Ethanol may be blocking the impulse flow mediated increase in dopamine synthesis. The hypothesis of Carlsson and Lindqvist (1973) that some of the central actions of ethanol could be mediated as a result of increased flow in central catecholamine-containing neurons is supported.