The 130th Annual Meeting of APHA

Abstract #51227

Christopher D. Toscano, Department of Environmental Health Sciences, Division of Toxicological Sciences, Johns Hopkins University Bloomberg School of Public Health, 615 N Wolfe Street, Room W2001, Baltimore, MD 21205, 410-955-7375, Chris_Toscano@hotmail.com

We have previously described that rats exposed to lead during gestation and lactation until weaning, exhibit deficits in spatial learning as young adults. Using this exposure protocol, we set out to determine if environmental enrichment (EE) altered the learning and molecular deficits induced by developmental exposure to lead. At weaning, male rats from control or lead-exposed litters were randomly assigned to isolated or EE housing. Rats were reared under these conditions until the end of spatial learning testing. Lead-exposed rats reared in isolation were markedly impaired in the acquisition of the spatial learning task at 50 days of age. However, lead- exposed rats reared in EE cages learned the spatial learning task as well as control EE rats. Recovery of learning performance in lead-exposed EE rats was associated with recovery of NMDA receptor (NMDAR) subunit 1 mRNA deficits and enhanced NMDAR levels in the hippocampus. Further, lead-exposed EE rats exhibited increased hippocampal expression of the nerve growth factor, brain-derived neurotrophic factor (BDNF). These findings demonstrate for the first time that cognitive and molecular deficits resulting from developmental exposure to lead are reversible by providing a social and enriched environment. Our studies provide a new direction for the treatment of children with cognitive deficits resulting from environmental exposure to lead.

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