Early Postnatal Ethanol Exposure Has Long‐Term Effects on the Performance of Male Rats in a Delayed Matching‐to‐Place Task in the Morris Water Maze

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There is concern that, in the absence of full-blown fetal alcohol syndrome, binge drinking during pregnancy might produce long-term cognitive deficits in offspring. Spatial working memory might be particularly vulnerable in this regard. This is the first study to address this issue in an animal model of binge exposure during the brain growth spurt using a delayed matching-to-place (DMTP) task in the Morris water maze. Infant male rats were gastrostomized and reared artificially from postnatal days (PD) 5 to 18. From PD 6 to 9 they were fed either 6.5 g x kg(-1) x d (-1) ethanol (EtOH) in a binge exposure model (BAC 302 mg/dl) or an isocaloric maltose-dextrin solution (MD). The study included a third suckled control group (SC) that was reared normally. The rats were tested on a series of problems in the DMTP task, first as juveniles (PD 35) and then twice again as adults. Each problem included an initial search trial and a subsequent test trial. The first two phases of testing used delays of either 0 sec or 60 sec between these two trials. The third phase increased this delay to 60 sec and 2 hr. In addition, the rats were tested on a cued task in the water maze. EtOH rats were impaired relative to controls in their ability to relocate the hidden platform on the second trial, which followed the search trial. In Phases 1 and 2, there was no differential effect of ethanol on performance across the 0-sec and 60-sec delay conditions. However, EtOH rats were more affected by the longer 2-hr delay in Phase 3. There were no group differences on the search trial, in swimming speed, or cued-task performance. These findings establish that binge exposure to ethanol during the brain growth spurt results in a long-lasting impairment on the DMTP performance of rats in the water maze.