Ascorbic acid effect on ethanol sensitivity via possible dopaminergic mediation.

Substance and alcohol actions/misuse Pub Date : 1984-01-01
J Yanai, R H Fishman, L Mittleman
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Abstract

Mice were injected with 0, 107, 215, 430, or 1720 mg/kg of ascorbic acid. Thirty min later they were tested for ethanol (3.5 g/kg) induced sleep time. Brain ethanol levels were determined upon awakening. Another group of mice were tested for apomorphine (3 mg/kg) induced locomotor activity also 30 min after ascorbic acid injection. Ascorbic acid in doses above 215 mg/kg augmented ethanol sleep time up to 210% at the highest doses, the increase being significant from 430 mg/kg. Brain ethanol levels upon awakening were reduced by ascorbic acid treatment; this reduction was significant at 1720 mg/kg dose. Ascorbic acid decreased apomorphine-induced locomotor activity in a dose response manner that paralleled the ascorbic acid increase of ethanol sleep time. At the highest dose of ascorbic acid, apomorphine-induced locomotor activity was completely eliminated. It is suggested that ascorbic acid increases brain sensitivity to ethanol by lowering the activity of dopamine receptors.

抗坏血酸对乙醇敏感性的影响可能通过多巴胺能介导。
小鼠分别注射0、107、215、430或1720 mg/kg的抗坏血酸。30分钟后,测试乙醇(3.5 g/kg)诱导的睡眠时间。醒后测定脑乙醇水平。另一组小鼠注射抗坏血酸30 min后,检测阿波啡(3 mg/kg)诱导的运动活性。抗坏血酸剂量高于215 mg/kg时,乙醇睡眠时间在最高剂量下可增加210%,从430 mg/kg开始显著增加。抗坏血酸治疗可降低醒后脑乙醇水平;在1720 mg/kg剂量下,这种减少是显著的。抗坏血酸降低阿吗啡诱导的运动活性,其剂量反应方式与抗坏血酸增加乙醇睡眠时间平行。在最高剂量的抗坏血酸下,阿吗啡诱导的运动活性完全消除。这表明抗坏血酸通过降低多巴胺受体的活性来增加大脑对乙醇的敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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