产后抑郁（PPD）严重威胁产妇与新生儿健康，发病机制未明且尚无有效的治疗方法，探究其防治新策略和药物新靶点是临床热点。研究证实，激活转位蛋白18KDa（TSPO）可显著增强GABA传导功能，表现出抗抑郁效应。我们前期研究发现，应用TSPO激动剂可以显著缓解PPD小鼠抑郁样行为，兼有神经保护、抗焦虑、改善脑缺血再灌注损伤的作用；电生理记录发现TSPO激动剂显著增强PPD小鼠外侧僵核（LHb）GABAA受体介导的抑制性传递，并且不影响小鼠新物体识别的学习记忆能力。提示TSPO可作为PPD的潜在药物治疗靶点。据此本项目首次提出，激活TSPO调控LHb中GABA能抑制性传递具有抗PPD的作用。本项目拟采用多种研究技术，探讨PPD发病时LHb中TSPO介导抑制性神经传递紊乱的作用及其机制。为揭示PPD发病的新机制，发现治疗PPD药物作用新靶点，研发新型PPD防治药提供新的思路。

Postpartum depression (PPD) is a severe mental disorder and threat to maternal and neonatal health, however, the mechanisms involved in the development of PPD are still unclear and there are no specific targets for the treatment. Therefore, it is very important to explore the new strategies for prevention and therapy of PPD, as well as targets for clinical treatment. Evidence showed that activation of translocator protein 18KDa (TSPO) exhibited antidepressant effects by enhancing GABAergic transmission. Our previous data showed that that activation of TSPO significantly alleviated the PPD mice depression- and anxiety-like behaviors. Electrophysiological recordings revealed that activation of TSPO promoted the excitability of the GABAergic neurons in the lateral Habenula nucleus (LHb), but not affected the novel object recognition ability of mice. This implicates the potential antidepressant effects of activation of TSPO is through enhancing the inhibitory neural transmission. This project firstly proposes that activation of TSPO exerts antidepressant effects by enhancing GABAergic transmission in the LHb. We will combine mutiple methods, including behavioral tests, electrophysiological recordings, and molecular biology, to investigate the roles of TSPO in PPD and the underlying mechanisms. The research will help to elucidate the pathological mechanisms of PPD and provide new potential targets for PPD.