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Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure
Author(s) -
Guilarte Tomás R.,
Toscano Christopher D.,
McGlothan Jennifer L.,
Weaver Shelley A.
Publication year - 2003
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.10399
Subject(s) - environmental enrichment , neurotrophic factors , hippocampus , brain derived neurotrophic factor , psychology , nmda receptor , protein subunit , receptor , cognition , gene expression , endocrinology , neuroscience , medicine , biology , gene , biochemistry
Long‐term deficits in cognitive function are the principal effects of lead (Pb 2+ ) exposure in children and can be modeled in experimental animals. Current therapeutic approaches in the treatment of childhood Pb 2+ 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 Pb 2+ exposure in rats. Enhanced learning performance of Pb 2+ ‐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 Pb 2+ ‐exposed animals and was present in the absence of changes in the NR2B subunit of the N‐ methyl‐ D ‐aspartate receptor, GluR1, αCamKII, 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 Pb 2+ 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 Pb 2+ intoxication.