Chronic ethanol consumption induces tolerance to the spatial memory impairing effects of acute ethanol administration in rats.

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.