Neonatal lead exposure in rats: II. Effects on the hippocampal afterdischarge

Male Sprague-Dawley rats were exposed to lead from parturition to weaning via the dams' milk. Dams were provided with drinking water containing 1.0 (LL), 2.5 (ML), or 5.0 (HL) mg/ml lead acetate or 1.25 (C) mg/ml sodium acetate. Beginning at 15 weeks of age, characteristics of the electrically elicited hippocampal afterdischarge (AD) and its alteration by phenytoin (PHT) were assessed in these rats. A separate group of rats was sacrificed at 20 weeks for hippocampal metal analysis. Increases in primary AD duration were observed in LL and ML, significant in ML. Significantly fewer wet dog shakes occurred in all lead groups. HL animals displayed shorter rebound ADs. All groups responded to PHT with increases in primary AD duration, but the increases in the ML and HL groups were significantly greater than in the C group. Hippocampal lead, zinc, and copper were not different from control. It is concluded that a brief lead exposure can have persistent effects on hippocampal function and that these effects are not due to altered hippocampal metal concentrations. The findings are discussed in relation to the known effects of postnatal lead exposure on hippocampal neuronal development.