目的研究创伤后应激障碍(PTsD)祥大鼠中缝背核神经元细胞凋亡及三偏磷酸酶(TMP)活性的表达变化。方法采用SPS刺激方法,建立PTSD样大鼠SPS模型,随机分为SPS刺激后1d、7d、14d和正常对照组,应用AnnexinV—FITC/PI双标记流式细胞术、透射电镜和酶组化方法,分;引对各组中缝背核神经元细胞凋亡及其TMP活性变化的观察和定量检测。结果SPS刺激后1d、7d、14d中缝背核神经元出现了细胞凋亡的特征性形态学改变、其凋亡率明显增加、TMP活性表达明显比正常对照组增强,并于7d达到高峰。结论PTSD样大鼠中缝背核神经元细胞出现凋亡,凋亡率增加的同时TMP活性增强,提示TMP参与了中缝背核神经元细胞的凋亡产物的降解与处理过程,脑桥体积缩小可能与中缝背核神经元细胞凋亡有关。
Objective To study expression of TMP activity and apoptosis in the dorsal raphe nucleus of P-ISD (posttraumatic stress disorder) mrs. Methods The SPS-roetbod was used to set up the rat PTSD models. Rats were randomly divided into 1d, 7d and 14d groups of SPS and normal group. Apoptosis in the dorsal raphe nucleus were detected by using annexin V-FITC/PI double-labled flow cytoroetry. The changes of TMP activity in the dorsal raphe were detected by light microscope and transmission electron microscopy (TEM). Results SPS exposure resulted in a significant change of characteristic roorphologic changes of apoptosis in the dorsal raphe nucleus. Apoptosis rate in dorsal raphe nucleus was significantly increased and TMP activity was significantly enhanced compared with that of normal control group (P 〈 0.05 ). Both markers reached the peak at 7 d after SPS exposure. Conclusion Dorsal raphe neurons of PTSD rats have had appotosis. The changes of apoptosis rate and TMP activity enhanced enhancing may might indicate that the TMP is was involved in degradation and processing of the apoptotic product in dorsal raphe nucleus, and smaller volume of pans may might be related to appotosis of dorsal raphe nucleus.