刺五加总苷对REM睡眠剥夺所致大鼠记忆获得障碍的改善作用及其LTP机制

目的： 研究刺五加总苷对快动眼睡眠剥夺（REMSD）所致记忆获得障碍的改善作用及对突触电位长时程增强（LTP）的影响，探讨刺五加总苷改善学习记忆能力的可能机制。 方法： 成年雄性SD大鼠，随机分为大平台对照组、睡眠剥夺组和刺五加总苷3个剂量组（200，100，50 mg·kg^-1）。各组大鼠灌胃给药/蒸馏水3 d后，利用改良多平台水环境法（MMPM）剥夺REM睡眠，制备学习记忆获得障碍动物模型；造模期间利用六角迷宫进行训练并测试，观察刺五加总苷对记忆获得障碍的改善作用；最后利用电生理学方法，高频刺激大鼠海马内嗅皮层穿通纤维诱导LTP，记录海马齿状回颗粒细胞层群峰电位（PS ）幅值。 结果： 与对照组相比，模型组大鼠的记忆能力降低（P<0.01），同时伴有海马脑区强直刺激后PS幅值明显下降（P<0.01）；与模型组大鼠相比，刺五加总苷中、高剂量均能明显增强模型大鼠的记忆能力（P<0.05，P<0.01）。升高PS幅值（P<0.01，P<0.05），且具有剂量依赖性。 结论： REM睡眠剥夺能够造成大鼠记忆获得障碍，刺五加总苷能够改善这种障碍，此作用可能与增强大鼠海马区突触可塑性有关。

Effect of Total Glucosides of Acanthopanax senticosus on Memory Acquisition Deficit Rats Induced by REM Sleep Deprivation and It's LTP Mechanism

Objective: To observe the effect of total glycosides of Acanthopanax senticosus on memory acquisition deficit induced by rapid eye movement sleep deprivation(REMSD)and illustrate the underlying mechanism of long-term potentiation(LTP) and synaptic plasticity. Method: Male SD ratswere used in this study. Rats were deprived of REM sleep by modified multiple platform method (MMPM).The REM sleep loss before learning could result in memory acquisition deficit in rats. Then we investigated the effect of total glycosides of A.senticosus on memory acquisition deficit rats with hexagonal maze paradigm. At last, the population spike (PS)amplitudein the hippocampus (CA1) region of the rats was recordedwith electrophysiological technic in vivo. Result: Compared with control group,the ability of learning and memory as well as PS amplitude obviously descended in model group(P<0.01). Those in two doses of total glycoside of A.senticosus(200, 100 mg·kg^-1)were enhanced significantly compared with model group(P<0.01 or P<0.05) in a dose-dependent manner. Conclusion: REMSD before learning could cause memory acquisition deficit. Total glycosides of A.senticosus could protect the memory deficitcaused by REMSD. The protective effect may be related to the enhanced synaptic plasticity in the hippocampus CA1 regionof rats.