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$pm$98 and $270{pm}46$ ng Pb/g, respectively The control group showed the background level of Pb ($3.7{pm}1.0_{ng}$ 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 $18:2_{n-6}$, $20:2_{n-6}$ and $18:2_{n-6}$ were decreased in the Pb-treated group with an increase in $20:4_{n-6}$ 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.