脑卒中后抑郁(PSD)是脑卒中后常见的并发症，严重影响卒中患者的神经功能恢复和社会生活。最新研究表明 Gadd45b介导的DNA去甲基化通路可促进大脑神经再生及可塑性，在脑缺血及许多精神疾病中发挥核心调控作用，但其在卒中后抑郁中的作用尚不清楚。本课题前期研究证实Gadd45b介导BDNF启动子去甲基化促进脑缺血后神经可塑性及神经功能恢复。本研究建立大鼠PSD模型，研究Gadd45b 表达及其调控对卒中后抑郁大鼠行为学，海马BDNF启动子甲基化状态及海马神经再生及可塑性的影响。从整体、组织和分子水平探讨Gadd45b 在PSD的调控作用及机制，藉此为PSD补充治疗方式研究提供理论依据。

As the common neuropsychiatric consequence of stroke, post-stroke depression (PSD) leads to the increases in their physical disability and even mortality. Emegring studies showed that Gadd45b-mediated DNA demethylation pathway can promote neurogenisis and long-term brain plasticity. Gadd45b plays an important role in ischemic cerebral stroke and many major psychosis. However, it is unknown whethe Gadd45b contribute the pathogenesis of PSD. Our preliminary study showed that Gadd45b-mediated BDNF promoter demethylation promote neural plasticity and function recovery in ischemic stroke. This study plan to adobt rat PSD, studies the impact of regulation and control of Gadd45b expression (inhibited by RNAi, promoted by electroconvulsive shock ) on behavioral effects, hippocampal neurogenesis and plasticity and BDNF promoter methylation level. We explore the mechanism of Gadd45b in regulating PSD from the whole, tissue and molecular levels. We hope to find a theoretical basis for the rehabilitation of patients with PSD by this study.