Abstract
The effect of acetaldehyde (0.7 g/kg, orally) or 4-methylpyrazole (8 mg/kg i.p.) and ethanol (7 g/kg orally) on the net accumulation of 3H-catecholamines (3H-CA) formed from 3H-tyrosine in the mouse brain was studied. Both drug regimens increased the yield of 3H-CA, similar to previous findings with ethanol alone. The effect of acetaldehyde was prevented by pretreatment with nialamide (100 mg/kg i.p.), a monoamine oxidase inhibitor. The ethanol-induced increase in 3H-CA accumulation was, if anything, enhanced by pretreatment with 4-methylpyrazole, which inhibits alcohol dehydrogenase. Acetaldehyde (100 mg/kg i.v.) and possibly, to some extent, ethanol (2 g/kg i.v.) released 14C-octopamine formed from 14C-tyramine in the mouse heart, whereas neither of the drugs (in the same doses) seemed to release “reserpine-resistant” 3H-noradrenaline from the mouse heart, an effect obtained by d-amphetamine (0.2 mg/kg i.v.). Pretreatment with 4-methylpyrazole (8 mg/kg i.p.) potentiated the stimulant action of ethanol (2 g/kg i.p.) on motor activity in the mouse. It is concluded that: 1. Acetaldehyde is not necessary to obtain the effects of ethanol on 3H-CA-accumulation and motor activity in the mouse. 2. The slight CA-releasing effect of ethanol and acetaldehyde is different from that of low doses of amphetamine and may possibly imply release of amines from the storage granules.
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Svensson, T.H., Waldeck, B. Significance of acetaldehyde in ethanol-induced effects on catecholamine metabolism and motor activity in the mouse. Psychopharmacologia 31, 229–238 (1973). https://doi.org/10.1007/BF00422513
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DOI: https://doi.org/10.1007/BF00422513