Boulouard Michel, Lelong Véronique, Daoust Martine, Naassila Mickaël
Laboratoire de Pharmacologie, CERMN, UPRESS EA 2126, Université de Caen, UFR des Sciences Pharmaceutiques, 1, rue Vaubénard, France.
Behav Brain Res. 2002 Oct 17;136(1):239-46. doi: 10.1016/s0166-4328(02)00134-1.
A large number of studies in rats have investigated the effects of acute and chronic ethanol administration on performance on many spatial learning and memory tasks. However, no study has addressed the problem of whether chronic ethanol consumption induces tolerance to acute ethanol-induced spatial memory deficits. In this study, we analyzed the behavioral effects of acute ethanol administration on spatial memory and locomotor activity in rats chronically intoxicated by ethanol. Male Sprague-Dawley rats were given as their only available liquid source a 10% (v/v) aqueous ethanol solution for 2 weeks before behavioral testing and during the 1-week behavioral testing period. They were treated intraperitoneally with 1.5 g/kg of ethanol 30 min before daily training in the Morris water maze, a spatial memory task sensitive to hippocampal damage. Our results demonstrate that learning and spatial memory of ethanol-consuming animals were not altered compared with control rats. Chronic ethanol consumption had no effect on spatial reference memory in terms of either the distance traveled to find the hidden platform during the acquisition phase of the experiment, or the time spent in the training quadrant during the retention trial. Acute ethanol administration impaired spatial memory in control rats and this impairment was reversed in chronic ethanol-consuming animals, revealing that chronic ethanol consumption did induce tolerance to the spatial memory deficits induced by acute ethanol injection, although plasma ethanol levels did not differ between the two groups. In contrast, chronic ethanol consumption did not induce tolerance to the acute ethanol-induced stimulatory locomotor activity measured in the same animals. Our results, therefore, indicate that chronic ethanol consumption induces tolerance to the cognitive impairing effects, but not to the locomotor stimulatory effects of acute ethanol administration in rats, suggesting that these two behavioral effects of ethanol do not share a common mechanism in the CNS.
大量针对大鼠的研究探讨了急性和慢性给予乙醇对多种空间学习和记忆任务表现的影响。然而,尚无研究探讨慢性乙醇摄入是否会诱导对急性乙醇所致空间记忆缺陷的耐受性这一问题。在本研究中,我们分析了急性给予乙醇对长期乙醇中毒大鼠空间记忆和运动活动的行为学影响。雄性Sprague-Dawley大鼠在行为测试前2周以及为期1周的行为测试期间,仅给予10%(体积/体积)乙醇水溶液作为唯一可用的液体来源。在每天进行对海马损伤敏感的空间记忆任务——Morris水迷宫训练前30分钟,给它们腹腔注射1.5 g/kg乙醇。我们的结果表明,与对照大鼠相比,饮酒动物的学习和空间记忆没有改变。在实验的获取阶段,慢性乙醇摄入对寻找隐藏平台所行进的距离,或在记忆测试期间在训练象限所花费的时间方面的空间参考记忆均无影响。急性给予乙醇会损害对照大鼠的空间记忆,而这种损害在长期饮酒的动物中得到逆转,这表明慢性乙醇摄入确实诱导了对急性乙醇注射所致空间记忆缺陷的耐受性,尽管两组之间的血浆乙醇水平并无差异。相比之下,慢性乙醇摄入并未诱导对在同一动物中测量的急性乙醇所致刺激性运动活动的耐受性。因此,我们的结果表明,慢性乙醇摄入诱导了对急性乙醇给药的认知损害作用的耐受性,但未诱导对其运动刺激作用的耐受性,这表明乙醇的这两种行为效应在中枢神经系统中不共享共同机制。