【摘要】 目的　对纳洛酮改善东莨菪碱所致大鼠空间工作记忆障碍的神经机制进行探索。目的　对纳洛酮改善东莨菪碱所致大鼠空间工作记忆障碍的神经机制进行探索。方法　大鼠随机分成三组:正常组、东莨菪碱组和纳洛酮治疗组,采用Morris水迷宫延缓性匹配任务试验记录每只大鼠前后两次逃避潜伏期的时间。利用免疫组化及图像分析技术,定量测定各组大鼠海马和前额叶皮层胆碱乙酰转移酶(ChAT)合成,利用电子显微镜技术,观察大鼠海马CA1区超微结构的改变。结果　(1)前后两次逃避潜伏期在正常组呈极显著性差异(t =7.32, P =0.00),东莨菪碱组无差异 (t =1.01, P =0.35),纳洛酮治疗组呈显著性差异(t =3.19, P =0.02)。(2)各组大鼠海马CA1、CA3区, 前额叶皮层神经元ChAT量无差别(P >0.05)。(3)各组大鼠锥体细胞胞体超微结构正常,但东莨菪碱组CA1区神经元突触超微结构明显改变。结论　M-型胆碱能受体阻滞剂东莨菪碱能损害大鼠空间工作记忆;阿片受体阻滞剂纳洛酮能够改善这种损害,其神经机制并非是增加 ChAT活性,而是能促进神经元突触囊泡Ach向突触间隙大量释放,及增加突触后致密物质密度。更多还原

【Abstract】 Objective To search for the neuro-mechanism of naloxone improving scopolamine-induced impairment of spatial working memory of rats in Morris water maze performance. Methods All naive rats were divided at random into three groups: normal group, scopolamine group and naloxone treatment group. The escape latencies were record in a delayed-matching to sample variant task. The expression level of ChAT in area of hippocampus and prefrontal lobe were assayed quantitatively by immunohistochemistry and the computerized image technique. The ultrastructure of neuronal pyramidal cells and formation of synaptic plasticity in hippocampus CA1 was observed under electron-microscope. Results The mean escape latencies of trial 2 and trial 1 were significantly different in normal group (t=7.32, P=0.00) and in naloxone treatment group (t=3.19, P=0.02), but not in scopolamine group (t=1.01, P=0.35). The quantity of ChAT in above area in three groups was not different statistically (P>0.05) and the ultrastructure of neuronal pyramidal cells in CA1 area was not changed. However, the synaptic plasticity alteration was found obviously in scopolamine group in hippocampal CA1 area. Conclusions Naloxone can improve the effect of scopolamine-induced impairment of spatial working memory in Morris water maze in rats. The neuromechanism may not enhance ChAT expression quality, but augmentation Ach exocytosis and post-synaptic density.更多还原