研究表明p75NTR通过调节mTOR介导的海马神经元凋亡、自噬及突触可塑性在PTSD共症与其他精神障碍行为及认知功能中发挥重要作用，提示其可能参与PTSD的发生。前期我们发现内源性p75NTR拮抗或敲除后PTSD动物行为及认知功能均得到有效改善，推断其在该过程中发挥重要作用，其机制可能与mTOR介导的海马神经元凋亡、自噬与突触改变有关。为验证该假设，本研究拟利用p75NTR拮抗大鼠及敲除小鼠PTSD模型，采用流式细胞术或TUNEL法结合组织病理检测海马神经元凋亡及自噬，通过检测p75NTR及凋亡、自噬相关基因表达分析他们之间的相关性；采用神经电生理法记录海马神经元LTD及LTP或通过检测海马突触可塑性标志物表达分析突触改变与p75NTR的关系；通过检测mTOR信号活性探讨p75NTR在PTSD致行为及认知功能障碍中的作用与机制，为PTSD发病机制研究提供有益补充，进而为其提供新的治疗靶点。

Studies have shown that p75NTR plays an important role in mTOR signal mediated apoptosis, autophagy and synaptic plasticity of hippocampal neurons in PTSD comorbidities and other neuropsychiatric diseases, suggesting that it may play an important role in the pathogenesis of PTSD. Our previous study found that the behavior and cognitive function of PTSD animal were improved effectively, when blocking or knockout endogenous p75NTR. Thus infered that p75NTR may play an important role in PTSD induced behavioral and cognitive disorders, and the mechanism may be related to mTOR signal mediated apoptosis, autophagy and synaptic plasticity in hippocampal neurons. In order to verify this hypothesis, in the present study, the PTSD animal models of p75NTR blocking rats and knockout mice will be used to investigate the apoptosis and autophagy of hippocampal neurons by using flow cytometry or TUNEL method, combined with pathological detection, and the expression of p75NTR, apoptosis and autophagy related gene will be detected in hippocampal neurons, then, the correlation between them will be analysised; Long-term depression (LTD) and long-term potentiation (LTP) in hippocampal neurons will be recorded by using the neural electrophysiological method, or the expression of hippocampal synaptic plasticity markers will be detected, and the relationship between the synaptic change and the expression of p75NTR will be further analysised; Through detection of the activity of mTOR signaling pathway, the role and mechanism of p75NTR in PTSD induced behavioral and cognitive dysfunction will be revealed, which will provide a useful supplement for the pathogenesis of PTSD and further provide a new therapeutic target for PTSD.