Rodd-Henricks Z A, McKinzie D L, Murphy J M, McBride W J, Lumeng L, Li T K
Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine and VA Medical Center, Indiana University-Purdue University at Indianapolis, 46202-4887, USA.
Alcohol Clin Exp Res. 2000 Jun;24(6):747-53.
The alcohol deprivation effect (ADE) is a temporary increase in the ratio of alcohol/total fluid intake and voluntary intake of ethanol (EtOH) solutions over baseline drinking conditions when EtOH access is reinstated after a period of alcohol deprivation. The ADE has been posited to be an animal model for alcohol craving. In the current study, we examined the effects of initial deprivation length and number of deprivation exposures on the ADE in the replicate lines of the high-alcohol-drinking (HAD) rats.
Adult male HAD-1 and HAD-2 rats received 24 hr free-choice access to 10% (v/v) EtOH and water for 6 weeks. Rats were then assigned to groups deprived of EtOH for 0 (control), or 2 to 8 weeks. All deprived groups were then given 24 hr access to EtOH for 2 weeks before being deprived of EtOH for another 2 weeks. This cycle of 2 weeks of access and 2 weeks of deprivation was carried out for a total of four deprivations.
After the initial EtOH deprivation period, EtOH consumption in HAD-1 and HAD-2 rats returned to baseline levels but failed to exhibit either an early onset ADE (initial 2 hr) or prolonged ADE (24 hr). An ADE was observed in two of the four deprived groups for the HAD-1 rats (2 week and 6 week groups) and in all deprived groups for the HAD-2 rats after a second deprivation, and in all deprived groups of both lines after a third deprivation. In the HAD-2 line, but not in the HAD-1 line, the duration of the ADE was prolonged into the second reinstatement day after the fourth deprivation.
The expression of an ADE was observed only after repeated deprivation periods in the HAD lines. The duration of the ADE was prolonged in the HAD-2 line, but not in the HAD-1 line, with repeated deprivations, which suggests a dissociation between selection for alcohol preference and the effects of repeated deprivations on the duration of the ADE.
酒精剥夺效应(ADE)是指在一段时间的酒精剥夺后恢复酒精摄入时,酒精/总液体摄入量的比例以及乙醇(EtOH)溶液的自愿摄入量相对于基线饮酒条件出现暂时增加的现象。ADE被认为是酒精渴望的动物模型。在本研究中,我们研究了初始剥夺时长和剥夺暴露次数对高酒精摄入(HAD)大鼠复制品系中ADE的影响。
成年雄性HAD-1和HAD-2大鼠可自由选择10%(v/v)EtOH和水,持续6周。然后将大鼠分为剥夺EtOH 0周(对照组)或2至8周的组。所有剥夺组在再给予24小时EtOH摄入2周后,再剥夺EtOH 2周。这种2周摄入和2周剥夺的循环共进行四次剥夺。
在最初的EtOH剥夺期后,HAD-1和HAD-2大鼠的EtOH消耗量恢复到基线水平,但未表现出早期ADE(最初2小时)或延长的ADE(24小时)。在第二次剥夺后,HAD-1大鼠的四个剥夺组中有两个组(2周和6周组)以及HAD-2大鼠的所有剥夺组观察到ADE,第三次剥夺后两个品系的所有剥夺组均观察到ADE。在HAD-2品系中,但不在HAD-1品系中,第四次剥夺后ADE的持续时间延长至第二次恢复日。
仅在HAD品系中经过重复剥夺期后才观察到ADE的表达。随着重复剥夺,HAD-2品系中ADE的持续时间延长,但HAD-1品系中未延长,这表明在酒精偏好选择与重复剥夺对ADE持续时间的影响之间存在分离。