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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure.

Authors: Guilarte, Tomás R; Toscano, Christopher D; McGlothan, Jennifer L; Weaver, Shelley A

Published In Ann Neurol, (2003 Jan)

Abstract: Long-term deficits in cognitive function are the principal effects of lead (Pb2+) exposure in children and can be modeled in experimental animals. Current therapeutic approaches in the treatment of childhood Pb2+ intoxication are not effective in reversing learning deficits once they have occurred. We report that environmental enrichment reverses long-term deficits in spatial learning produced by developmental Pb2+ exposure in rats. Enhanced learning performance of Pb2+-exposed animals reared in an enriched environment was associated with recovery of deficits in N-methyl-D-aspartate receptor subunit 1 (NR1) mRNA and induction of brain-derived neurotrophic factor (BDNF) mRNA in the hippocampus. The effect of environmental enrichment on NR1 and BDNF gene expression was specific to Pb2+-exposed animals and was present in the absence of changes in the NR2B subunit of the N-methyl-D-aspartate receptor, GluR1, alpha CamKII, or PSD-95 gene expression measured in the same animals. Our findings demonstrate that the learning impairments and NR1 subunit mRNA deficits resulting from developmental Pb2+ exposure are reversible if the animals are provided with an enriched environment even after the exposure has occurred. We propose environmental enrichment as a basis for the treatment of childhood Pb2+ intoxication.

PubMed ID: 12509847 Exiting the NIEHS site

MeSH Terms: Age Factors; Animals; Body Weight; Brain-Derived Neurotrophic Factor/genetics; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Calcium-Calmodulin-Dependent Protein Kinases/genetics; Cognition Disorders/physiopathology*; Cognition Disorders/therapy*; Conditioning (Psychology)/physiology; Disease Models, Animal; Disks Large Homolog 4 Protein; Environment*; Female; Gene Expression; Hippocampus/physiology; Intracellular Signaling Peptides and Proteins; Lead Poisoning, Nervous System/physiopathology*; Lead Poisoning, Nervous System/therapy*; Membrane Proteins; Nerve Tissue Proteins/genetics; Rats; Rats, Long-Evans; Receptors, AMPA/genetics; Receptors, N-Methyl-D-Aspartate/genetics; Space Perception/physiology

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