女性绝经期后，以焦虑为主要特征的更年期综合症发病明显增多，提示雌激素水平下降可能是焦虑发病的重要因素。雌激素替代治疗可有效缓解更年期综合症，但心血管和肿瘤风险限制了临床应用，因此，发掘新的治疗策略成为临床迫切需求。GPR30是一种新型雌激素膜受体。我们前期研究发现，与焦虑相关的杏仁核区域高表达GPR30；杏仁核局部给予GPR30激动剂G1可显著抑制小鼠焦虑样行为；电生理记录发现激动GPR30可显著增强杏仁核中间神经元的兴奋性，加强GABA介导的抑制性突触传递，提示GPR30在焦虑治疗中的潜在价值。本项目首次提出杏仁核雌激素膜受体GPR30能够快速调节GABA能抑制性传递，可成为抗焦虑药物作用的新靶点。本研究拟采用免疫组织化学、分子生物学、电生理和行为学等方法，探讨杏仁核GPR30与GABA能抑制性传递的关系，为研究焦虑症的发病机制及发掘抗焦虑药物作用新靶点提供理论依据。

The incidence of menopausal syndrome, which shows obvious anxiety in clinical, is significantly increased in post-menopausal women, suggesting that the decline of estrogen levels is an important factor for anxiety onset. Estrogen replacement therapy is effective to relieve menopausal symptoms; however, the cardiovascular and cancer risk limit the clinical application. Therefore, to explore new treatment strategies is clinically urgent demand. GPR30 is a novel estrogen membrane receptor. Our previous study found that GPR30 highly expressed in the anxiety-related amygdala region. Amygdala local infusion of GPR30 agonist G1 could significantly inhibit anxiety-like behavior. Further electrophysiological recording revealed that activation of GPR30 significantly increased the excitability of inhibitory neurons and enhanced the GABA-mediated inhibitory synaptic transmission, suggesting the potential value of GPR30 in the treatment of anxiety. Here, we firstly propose that estrogen membrane receptor GPR30 can quickly regulate the GABAergic inhibitory transmission, which can be a new target for anxiolytic drug. Multiple methods such as immunochemistry, molecular biology, electrophysiology, and behavioral test will be used to explore the relationship between GPR30 and GABA transmission. This project will be helpful to elucidate the mechanisms underlying the pathogenesis of anxiety disorders and to provide a theoretical basis for exploring new anxiolytic drug targets.