Guo Ya-Jing, Wen Jing, Wang Meng-Yu, Cheng Xiang-Kun, Chen Xin-Wang
Henan University of Chinese Medicine, Zhengzhou 450046, China.
College of Acu-moxibustion and Tuina, Henan University of Chinese Medicine, Zhengzhou 450000.
Zhen Ci Yan Jiu. 2024 Nov 25;49(11):1168-1173. doi: 10.13702/j.1000-0607.20230728.
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.
SD rats were randomly divided into normal, model, EA and sham EA groups (=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.
Compared with the normal group, the escaping latency of the positioning navigation experiment in the model group was prolonged (<0.05), the number of crossing the platform and the residence time in the target quadrant were decreased(<0.05), the density of dendritic spines in the hippocampal CA1 area was decreased (<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 (<0.05) in the model group. Compared with the model group, the escape latency of the positioning navigation experiment was shortened (<0.05), the number of crossing platforms and the time spent in the target quadrant were increased (<0.05), the density of dendritic spines in the hippocampal CA1 region was increased (<0.05), the morphology of synaptic improved, the protein expression levels of PSD95 and MeCP2 were increased (<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.
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.
观察电针（EA）对睡眠剥夺大鼠突触功能相关蛋白PSD95和MeCP2表达及突触超微结构的影响，以探讨其改善睡眠剥夺所致学习记忆能力的机制。
将SD大鼠随机分为正常组、模型组、电针组和假电针组（每组n = 10）。采用改良多平台水环境法制备睡眠剥夺模型。电针组大鼠在“百会”（GV20）和“大椎”（GV14）穴进行电针刺激，假电针组在上述穴位旁4 mm处浅刺，不给予电刺激。采用Morris水迷宫试验评估学习记忆能力。通过高尔基染色检测海马CA1区树突棘密度。用电子显微镜观察海马的突触超微结构。采用蛋白质免疫印迹法检测海马中PSD95和MeCP2的蛋白表达水平。
与正常组相比，模型组定位航行实验的逃避潜伏期延长（P < 0.05），穿越平台次数和在目标象限的停留时间减少（P < 0.05），海马CA1区树突棘密度降低（P < 0.05），突触数量减少，突触小体肿胀，突触结构模糊，突触间隙消失或变窄，模型组PSD95和MeCP2的蛋白表达水平显著降低（P < 0.05）。与模型组相比，电针组和假电针组定位航行实验的逃避潜伏期缩短（P < 0.05），穿越平台次数和在目标象限的停留时间增加（P < 0.05），海马CA1区树突棘密度增加（P < 0.05），突触形态改善，PSD95和MeCP2的蛋白表达水平升高（P < 0.01）。电针组上述指标的改善比假电针组更明显。
电针可改善睡眠剥夺大鼠的学习记忆能力，这可能与其调节突触相关蛋白PSD95和MeCP2的表达以及改善突触结构的功能有关。
