Rodd-Henricks Z A, McKinzie D L, Shaikh S R, 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, Indianapolis 46202-4887, USA.
Alcohol Clin Exp Res. 2000 Jan;24(1):8-16.
The alcohol deprivation effect (ADE) is a temporary increase in the ratio of ethanol/total fluid intake and the voluntary intake of ethanol solutions over baseline drinking conditions when ethanol access is reinstated after a period of alcohol deprivation. The ADE has been posited to be an animal model for alcohol craving. The current study examined the effects of initial deprivation length and number of deprivation exposures on the ADE in alcohol-preferring (P) rats.
Adult female P rats received 24-hr free-choice access to 10% (v/v) ethanol and water for 6 weeks. Rats were then randomly assigned to five groups deprived of ethanol for 0 (control), 2, 4, 6, or 8 weeks (W). All deprived groups were then given 24-hr access to ethanol for 2 weeks before being deprived of ethanol for another 2 weeks.
After the initial ethanol deprivation period, the deprived groups displayed a similar 2-fold ADE (e.g., 4-W group; 4.6 +/- 0.5 for baseline vs. 10.5 +/- 0.3 g/kg/day for the 1st reinstatement day) during the initial 24-hr period. Ethanol consumption began to return to control levels 48 (7.1 +/- 0.4 g/kg/day) and 72 (6.4 +/- 0.4 g/kg/day) hrs later. In addition, each deprived group showed increases in the ratio of ethanol/total fluid intake upon reinstatement, and there was a tendency for sustained higher ethanol intake ratios during the first 3 postexposure days for the 4-, 6-, and 8-W groups, but only during the first 2 reinstatement days for the 2-W group. The second deprivation did not increase the magnitude of the ADE over that observed in the first deprivation during the initial 24-hr period of re-exposure, but it did prolong the duration of the ADE into the 2nd and 3rd reinstatement day for the 2-, 4-, and 6-W groups and into the 5th reinstatement day for the 8-W group.
Equivalent robust ADEs can be seen in P rats with deprivation periods of 2-8 W, which suggests that the ADE has a rapid onset and is not affected by the durations of deprivation that were tested. The duration of the ADE was prolonged in P rats exposed to a second deprivation period, suggesting that factors associated with the ADE phenomenon could be strengthened by repeated deprivations.
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，乙醇/总液体摄入量的比例以及乙醇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。本研究考察了初始剥夺时长和剥夺暴露次数对嗜酒（P）大鼠ADE的影响。
成年雌性P大鼠可自由选择饮用10%（v/v）乙醇和水24小时，持续6周。然后将大鼠随机分为五组，分别剥夺乙醇0（对照组）、2、4、6或8周（W）。所有剥夺组在再次剥夺乙醇2周前，先给予24小时的乙醇饮用时间，为期2周。
在初始乙醇剥夺期后，剥夺组在最初24小时内表现出相似的2倍ADE（例如，4周组；基线时为4.6±0.5克/千克/天，恢复饮酒第一天为10.5±0.3克/千克/天）。48小时（7.1±0.4克/千克/天）和72小时（6.4±0.4克/千克/天）后，乙醇摄入量开始恢复到对照水平。此外，每组剥夺组在恢复饮酒时乙醇/总液体摄入量的比例均增加，4周、6周和8周组在暴露后的前3天乙醇摄入量比例持续较高，但2周组仅在恢复饮酒的前2天出现这种情况。第二次剥夺在重新暴露的最初24小时内并未使ADE的幅度超过第一次剥夺时观察到的幅度，但对于2周、4周和6周组，它确实将ADE的持续时间延长到了第二次和第三次恢复饮酒日，对于8周组则延长到了第五次恢复饮酒日。
在剥夺期为2 - 8周的P大鼠中可观察到相当强烈的ADE，这表明ADE起效迅速，且不受所测试的剥夺持续时间的影响。暴露于第二次剥夺期的P大鼠中ADE的持续时间延长，这表明与ADE现象相关的因素可能会因重复剥夺而得到加强。
