Objectives: To observe the effect of electroacupuncture (EA) on the expression of synaptic function related proteins PSD95 and MeCP2 and synaptic ultrastructure in sleep deprived rats, so as to explore its mechanism underlying improvement of learning and memory ability caused by sleep deprivation.
Methods: SD rats were randomly divided into normal, model, EA and sham EA groups (n=10). The sleep deprivation model was prepared by modified multi-platform water environment. Rats of the EA group received EA stimulation at "Baihui" (GV20) and "Dazhui" (GV14), while the sham EA group received shallow needling 4 mm away from the above acupoints without electrical stimulation. The learning and memory ability was evaluated with Morris water maze test. The density of dendritic spines in hippocampal CA1 region was detected by Golgi staining. The synaptic ultrastructure of hippocampus was observed by electron microscope. The protein expression levels of PSD95 and MeCP2 in hippocampus was detected by Western blot.
Results: Compared with the normal group, the escaping latency of the positioning navigation experiment in the model group was prolonged (P<0.05), the number of crossing the platform and the residence time in the target quadrant were decreased(P<0.05), the density of dendritic spines in the hippocampal CA1 area was decreased (P<0.05), the number of synapses was reduced, with swollen synaptosomes, blurred synaptic structure, disappeared and narrowed synaptic clefts, the protein expression levels of PSD95 and MeCP2 were significantly decreased (P<0.05) in the model group. Compared with the model group, the escape latency of the positioning navigation experiment was shortened (P<0.05), the number of crossing platforms and the time spent in the target quadrant were increased (P<0.05), the density of dendritic spines in the hippocampal CA1 region was increased (P<0.05), the morphology of synaptic improved, the protein expression levels of PSD95 and MeCP2 were increased (P<0.01) in the EA and sham EA groups. The improvement of the above indexes in EA group was more obvious than those in sham EA group.
Conclusions: EA can improve the learning and memory of sleep deprivation rats, which may be related to its function in regulating the expressions of synaptic related proteins PSD95 and MeCP2, and improving the synaptic structure.
目的: 观察电针对睡眠剥夺大鼠突触功能相关蛋白突触后致密蛋白95（PSD95）、甲基CpG结合蛋白2（MeCP2）及突触超微结构的影响，探讨电针改善睡眠剥夺所致学习记忆能力下降的机制。方法: SD大鼠随机分为正常组、模型组、电针组和假电针组，每组10只。采用改良多平台水环境法制备大鼠睡眠剥夺模型。电针组电针“百会”“大椎”，假电针组在“百会”“大椎”定位向外旁开4 mm处针刺，连接电针仪后不通电，两组均每日1次，每次15 min，治疗5 d。采用Morris水迷宫测试大鼠空间学习记忆能力；高尔基染色检测海马CA1区树突棘密度；投射电镜观察海马区突触超微结构；Western blot法检测海马区PSD95、MeCP2蛋白的表达。结果: 与正常组相比，模型组定位航行实验逃避潜伏期延长（P<0.05），穿越平台次数和目标象限停留时间减少（P<0.05），海马CA1区树突棘的密度下降（P<0.05），突触数量减少、突触小体肿胀、突触结构模糊、突触间隙变窄甚至消失，海马区PSD95、MeCP2的蛋白表达降低（P<0.05）。与模型组相比，电针组和假电针组定位航行实验逃避潜伏期缩短（P<0.05），穿越平台次数和目标象限停留时间增加（P<0.05），海马CA1区树突棘的密度增加（P<0.05），突触数量增加、突触小体轻度肿胀、突触结构较完整，海马区PSD95、MeCP2的蛋白表达升高（P<0.05，P<0.01）。电针组较假电针组上述指标改善更明显（P<0.05）。结论: 电针可改善睡眠剥夺大鼠学习记忆，其机制可能与调控突触相关蛋白PSD95、MeCP2，改善突触结构有关。.
Keywords: Electroacupuncture; MeCP2; PSD95; Sleep deprivation; Synaptic.