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The present studies investigate how acutely administered ethanol (ETOH) affects the use of spatial memory. Previous electrophysiological results have shown that acutely administered ETOH alters the firing of hippocampal neurons and that prenatal or chronic exposure to ETOH produces deficits on spatial learning tasks, tasks dependent on the hippocampus. In contrast, it has also been demonstrated that acutely administered ETOH does not impair spatial localization. In the current studies, rats were trained to perform a spatial or stimulus/response task under saline. After training, rats were injected with ETOH, and the use of spatial or stimulus/response memory was tested. Acutely administered ETOH impaired the use of spatial memory, but not the use of stimulus/response memory. Because the use of spatial memory requires an intact hippocampus, the present studies suggest that acutely administered ETOH selectively impairs behaviors dependent on the hippocampus.

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This study describes a new mechanism by which ethanol alters brain function and may impair performance on tasks requiring spatial navigation. Recording electrophysiological activity from single neurons in the awake, freely behaving animal, the present study shows that ethanol impairs the ability of place cells in the hippocampus to process spatial information. The impairment by ethanol in spatial processing of place cells was remarkably similar to the impairment produced by lesions of afferents to the hippocampus, except that the effect of ethanol was reversible. Since lesions to hippocampal afferents that alter spatial processing of place cells concomitantly impair spatial navigation, the present results suggest that ethanol similarly impairs spatial navigation by altering spatial processing of place cells. The present results have implications for the observation that ethanol impairs performance on navigational tasks that require spatial processing, such as automobile driving.

The present study compared the effects of ethanol and diazepam on a task that allows for the assessment of both spatial working memory and the acquisition of spatial information within each day. During the first trial of each day, subjects were shown the spatial location of a food reward on a six-arm radial-arm maze. During nine subsequent free-choice trials, subjects were reinforced for returning to that same spatial location. The location of the food reward varied across days. Thus, choosing correctly on any given trial required subjects to remember where food had been received during the previous trials of that day. The effects of ethanol and diazepam on working memory were assessed by analyzing the overall number of errors committed during the nine free-choice trials of each day. The effects of ethanol and diazepam on within-day acquisition were assessed by comparing the number of errors committed during the first three trials of each day to the number of errors committed during the last three trials of each day. Ethanol and diazepam both produced dose-dependent increases in working memory errors, and both did so without impairing within-day acquisition. The results of the present study provide further evidence of the similarities between the effects of ethanol and benzodiazepine receptor agonists on learning and memory, and are consistent with the hypothesis that ethanol's potentiation of GABA at GABAA receptors contributes to the learning and memory impairments produced by ethanol.