Developmental exposure to mercury chloride does not impair social behavior of C57BL/6 × BTBR F(1) mice.

The effects of mercury (Hg) on social behavior and the mechanisms involved remain unknown. This study shows that Hg chloride (HgCl(2)) exposure during fetal development does not impair social behavior of a mouse strain susceptible to environment-induced autistic-like behavior based on the parental phenotype. On the contrary, Hg exposure elevated the sociability of females. Since B6 mice are behaviorally normal and BTBR mice display low levels of sociability, the F(1) offspring (B6BF(1)) of female B6 mice and male BTBR mice were used to investigate their social behavior and the effects of Hg. Developmental Hg-treatment increased the serum IgG levels of the post-natal day (pnd) 21 offspring, but not pnd70 offspring or the B6 dams. After Hg treatment, there were negligible levels of serum IgG anti-brain antibodies (Ab) in the pnd21 and pnd70 offspring as well as their dams. However, Hg did elevate IgG deposition in multiple assayed brain regions of the pnd21 offspring, but the higher levels were no longer present at pnd70. Cytokine levels were not changed in pnd21 or pnd70 brain by Hg exposure, suggesting neuroinflammation was not induced. Social behavior was assayed at pnd70. Surprisingly, Hg-treatment significantly enhanced sociability of female B6BF(1) offspring, but not that of the male offspring. Our data indicates that developmental exposure to HgCl(2) did not impair social behavior of B6BF(1) offspring, but it enhanced the sociability of females, which was significantly lower in adult B6BF(1) females than B6BF(1) males in the absence of any Hg exposure.