Exposure to ethanol and nicotine during the brain growth spurt: spatial DMP performance in male rats

Male Long-Evans rats were reared artificially and, using a 2x2 design, were exposed from postnatal days (PD) 6-9 to ethanol (ET: 6.5 g kg(-1) day(-1) "binge" exposure) and/or nicotine bitartrate (NIC: 6 mg kg(-1) day(-1) continuous exposure) via gastrostomy tubes. Controls were administered maltose-dextrin in amounts isocaloric to ET and/or sodium bitartrate. A fifth suckled-control group was reared normally. NIC accelerated eye opening on PD 14; whereas ET delayed eye opening and hindlimb support on PD 16. Beginning in postnatal week 7, rats were tested on a spatial delayed matching-to-place (DMP) version of the Morris water maze, which entailed a series of problems, each consisting of search and recall trials, that required the rats to use extra-maze cues to locate a hidden escape platform. In Phase 1 of testing, the ET-exposed groups were impaired in the recall trials, but there was no effect of NIC. A longer encoding time (45 vs. 10 s) improved performance across all groups. In contrast, acute administration of NIC (0.1 mg/kg ip) immediately prior to testing in Phase 2 failed to improve performance in any group. In conclusion, these results confirm previous findings of impaired spatial DMP-task performance in ET-exposed rats and further suggest that these memory deficits are amenable to amelioration.