Abstract
Lead (Pb) exposure during development can produce neurological deficits. In this study, the effect of Pb exposure during neonatal development via lactation on anxiety of brain function was investigated. Long-Evans strain rats were raised through two generations. At the birth of the second generation, the dams were subdivided into two groups and supplied drinking water containing either 0.2% Pb (Pb-treated group) or sodium (Na, Control group) acetate until weaning. Rats were sacrificed at 3 (weaning) and 11 weeks (maturity) for brain Pb and fatty acid analysis. Motor activity and elevated plus maze tests were initiated at 9 weeks. The brains in the Pb-treated group at weaning and maturity contained 1486±98 and 270±46 ng Pb/g, respectively. The control group showed the background level of Pb (3.7±1.0 ng Pb/g) in both ages. The alterations in brain fatty acid composition induced by Pb exposure were more evident in 3 wks old than 11 wks old. For example, in 3 wks old, the percentages of 18:2n-6, 20:2n-6 and 20:3n-6 were decreased in the Pb-treated group with an increase in 20:4n-6. In motor activity test, there was a tendency of hyperactivity in the Pb-treated group compared with the control group but the difference was not significant. In elevated plus maze test, the Pb-treated group showed fewer numbers of visits to the open arms (P<0.05), indicating that Pb exposure may lead to anxiogenic effect.
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