Previous reports have suggested a relationship between the neurotoxicity of lead and hippocampal dysfunction. Therefore, a comparison between the behavioral changes induced by lead exposure and by selective destruction of hippocampal neurons should help to clarify whether the intrinsic neurons of the hippocampus are directly influenced by lead. Rats maternally and permanently exposed to lead (750 ppm in the diet as lead acetate) were tested in a radial arm maze and compared with controls and rats with ibotenic acid-induced neuronal depletion in the dorsal hippocampus. Lead-exposed groups showed an impairment in the acquisition performance of the spatial task while hippocampally damaged animals did not. When they were retested 4 weeks after the end of the original acquisition, both groups of lead-exposed and ibotenic acid-treated rats showed a significant deficit in retention. These results suggest that this deficit produced by lead can be due to the damage of the hippocampal neurons but not the impairment observed in the acquisition. We propose that the neurotoxicity of lead is not entirely due to the dysfunction of the dorsal hippocampus and that other areas of the brain should be considered. Both maternally and permanently lead-exposed rats showed a similar degree of deficit in acquisition and retention, suggesting a long-lasting effect of early lead exposure.