Electrophysiology of hippocampal CA1 neurons after prenatal ethanol exposure

被引:34
作者
Krahl, SE
Berman, RF
Hannigan, JH
机构
[1] Wayne State Univ, CS Mott Ctr Human Growth & Dev, Dept Obstet & Gynecol, Detroit, MI USA
[2] Wayne State Univ, CS Mott Ctr Human Growth & Dev, Dept Psychol, Detroit, MI USA
关键词
fetal alcohol syndrome; FAS; hippocampus;
D O I
10.1016/S0741-8329(98)00043-3
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
In the present study, we examined the longitudinal effects of prenatal ethanol exposure on the electrophysiological characteristics of CAL neurons in hippocampal slices. Hippocampal slices were obtained from young (25-32-day old) and adult (63-77-day old) male offspring of rats given one of four treatments during gestation. Three groups of pregnant rats were orally intubated with 0, 4, or 6 g/kg ethanol on gestational days 8-20. Caloric intake for the 0- (nutritional control) and 4-g/kg groups was yoked to that of the 6 g/kg group. A fourth group (untreated control) was not intubated, and was given ad lib access to food. Long-term potentiation and paired-pulse inhibition were unaffected by prenatal ethanol exposure in young and adult rats; however, slices taken from the young 6 g/kg ethanol group displayed a significantly lower maximal CA1 population spike amplitude evoked by Schaffer collateral stimulation as compared to young controls. This difference was not observed in adult animals. These data suggest that some aspects of hippocampal physiology are negatively affected in young rats as a result of prenatal ethanol exposure, but this effect reverses as the animal matures. (C) 1999 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:125 / 131
页数:7
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