巴氯芬对撒丁岛嗜酒（sP）大鼠酒精戒断效应的抑制作用
Suppression by baclofen of alcohol deprivation effect in Sardinian alcohol-preferring (sP) rats.
作者信息
Colombo Giancarlo, Serra Salvatore, Brunetti Giuliana, Vacca Giovanni, Carai Mauro A M, Gessa Gian Luigi
机构信息
C.N.R. Institute for Neurogenetics and Neuropharmacology, c/o 'Bernard B. Brodie' Department of Neuroscience, University of Cagliari, S.S. 554, Km. 4.5, I-09042, Monserrato, CA, Italy.
出版信息
Drug Alcohol Depend. 2003 May 1;70(1):105-8. doi: 10.1016/s0376-8716(02)00333-2.
Alcohol deprivation effect (ADE), i.e. the transient increase in alcohol intake that takes place in laboratory animals after a period of alcohol deprivation, has been proposed to model alcohol relapses in alcoholics. The present study investigated the effect of the GABA(B) receptor agonist, baclofen, on the development of ADE in selectively bred Sardinian alcohol-preferring (sP) rats. Acute administration of non-sedative doses of baclofen (0, 1, 1.7 and 3 mg/kg, i.p.) resulted in the complete suppression of the extra-amount of alcohol consumed during the first hour of re-access to alcohol after 7 days of deprivation. These results implicate the GABA(B) receptor in the neural substrate mediating ADE and suggest that baclofen may possess anti-relapse properties.
酒精戒断效应（ADE），即在实验动物经历一段时间的酒精剥夺后出现的酒精摄入量短暂增加，已被提出用于模拟酗酒者的酒精复吸情况。本研究调查了γ-氨基丁酸B（GABA(B)）受体激动剂巴氯芬对选择性培育的撒丁岛嗜酒（sP）大鼠ADE发展的影响。急性给予非镇静剂量的巴氯芬（0、1、1.7和3毫克/千克，腹腔注射）导致在剥夺7天后重新接触酒精的第一小时内，额外摄入的酒精量被完全抑制。这些结果表明GABA(B)受体参与介导ADE的神经基质，并提示巴氯芬可能具有抗复吸特性。
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