Neuronal depletion of the amygdala resembles the learning deficits induced by low level lead exposure in rats

Abstract

The behavioral deficits observed after lead exposure have been related to limbic system dysfunction. In a previous study it was shown that the neurotoxicity of lead could not be explained by the damage of the hippocampus alone. The purpose of the present investigation was to use behavioral comparisons to test the hypothesis that the intrinsic neurons of several nuclei of the amygdala, where lead has been found to accumulate, can be a target of the effects of the metal as well. A group of rats were maternally and permanently exposed to lead (750 ppm in the diet as lead acetate). Another group of equally aged and housed rats, never experimentally exposed to lead, were injected ibotenic acid into the amygdala. All groups plus sham-operated and unoperated controls were tested in the open field, the radial arm maze, and a passive avoidance task. The results showed that lead exposure (both permanent and maternal) and amygdalectomy produced a) no effect on locomotor activity, b) impairments in the acquisition phase of the radial maze, and c) impairments in passive avoidance. These results suggest an involvement of the amygdala in the neurotoxic action of lead, but not as the only brain structure. The deficits in permanently lead-exposed rats are more pronounced than in only maternally-exposed animals suggesting a longlasting, but not totally irreversible effect of early lead exposure.