杏仁核BLA/CeA亚区 GABAergic中间神经元缺失介导PTSD恐惧记忆泛化及补肾填精治法的干预作用研究

目前，创伤后应激障碍（PTSD）的发病率显著增加，已成为本世纪最主要的公共健康卫生问题之一。作为PTSD的核心症状之一，恐惧记忆泛化（FMG）的研究对PTSD的防治具有重要的意义。杏仁核是处理和传播恐惧相关信号的关键区域，并具有显著的亚区和亚细胞群特点。GABAergic中间神经元的缺失可导致杏仁核的高兴奋性，使“兴奋－抑制”稳态失衡，这可能是FMG形成的重要机制。本研究采用单一延长应激建立PTSD大鼠模型，试图阐明杏仁核BLA/CeA亚区GABAergic中间神经元（包括PV、SST、CR亚型）缺失对FMG形成的影响及其机制；明确补肾填精治法逆转杏仁核GABAergic中间神经元缺失发挥抗FMG的效应以及是否存在脑区和亚细胞作用的特异性。本研究不仅为补肾填精治法方药防治PTSD的转化医学研究提供科学依据，而且将进一步揭示补肾填精治法在防治精神心理疾病中的科学价值及其特色和优势。

At present, the incidence of post-traumatic stress disorder (PTSD) has increased significantly and has become one of the major public health problems in this century. As one of the core symptoms of PTSD, the study of fear memory generalization (FMG) is of great significance for the prevention and treatment of PTSD. The amygdala is a key region for processing and spreading fear-related signals, and is characterized by distinct subregions and subcell populations. The loss of GABAergic intermediate neurons can lead to the high excitability of the amygdala, resulting in the imbalance of "excitation-inhibition" homeostasis, which may be an important mechanism for the formation of FMG. In this study, single prolonged stress was used to establish a PTSD rat model, in an attempt to elucidate the effect of loss of GABAergic intermediate neurons (including PV, SST and CR subtypes) in the BLA/CeA subregion of the amygdala on the formation of FMG and its mechanism. To clarify the specificity of the anti-FMG effect and the existence of brain region and subcellular function of the reverse amygdala GABAergic intermediate neuron loss by Bushentianjing therapy. This study not only provides a scientific basis for the translational medicine research on the treatment of prescription with Bushentianjing therapy in the prevention and treatment of PTSD, but also further reveals the scientific value, characteristics and advantages of Bushentianjing therapy in the treatment of mental and psychological diseases.