自闭症是一组以社会交流互动缺陷和具有某些重复性行为为特点的社会行为障碍的统称。其发病率逐年增高，但发病机制尚不清楚。由于流行病学调查结果的不一致，汞与自闭症的发病关系没有明确的结论。在小鼠模型中，我们先前的工作首次表明无机汞在一定条件下可通过母体的自身免疫环境诱导子代的自闭症行为。本课题的研究目标为利用小鼠模型进一步探索汞诱导自闭症行为的条件和机制。课题假设为无机汞对大脑的直接毒性作用并不引起自闭症行为，但在对汞敏感的个体，怀孕期和哺乳期接触无机汞可通过诱导母体产生对脑抗体从而造成子代的自闭症行为；不同个体对无机汞诱导的对脑抗体具有不同反应性。发育期通过母体接触甲基汞可能在自闭症易感个体中通过其直接毒性诱导自闭症行为。本研究将进一步深化对汞与自闭症发病关系的认识，为未来新开展的流行病学研究提供信息参考，同时也为自闭症的预防和治疗提供线索。

Autism Spectrum Disorders (ASD) refer to a group of neurodevelopmental disorders characterized by impaired social communication, deficient social interaction, and repetitive behaviors. The incidence of ASD has substantially increased, yet the mechanisms are not well defined. To date, due to contradictory epidemiological results, whether mercury (Hg) exposure causes or contributes to ASD is still inconclusive. Previously, we reported that Hg2+ exposure induces ASD-like behaviors in F1 offspring through activation of maternal autoimmune response in mouse models. The aim of this study is to further explore the influence and mechanism(s) of Hg effects on ASD-like behaviors. Herein, we hypothesize that Hg2+ exposure to dams sensitive to Hg-induced autoimmunity during pregnancy and lactation causes ASD-like behaviors in offspring via induction of maternal-derived anti-brain antibodies, rather than through direct Hg2+ toxicity to the brain. The effects of Hg2+-induced anti-brain antibodies on ASD-like behaviors vary dependent on genetic predispositions of offspring. In contrast, maternal methyl Hg exposure may induce impaired social behaviors in offspring susceptible to ASD, through direct interaction with the brain. Our study will promote the fundamental understanding of the relationship between Hg exposure and ASD-like behaviors and provide new strategies for future epidemiological studies as well as ASD control and treatment.