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作 者:王璐[1] 霍帅[1] 王亚飞[2] 赵琳[1] 刘伯锋[1] 阮彩莲[1] 惠雪枫[1]
机构地区:[1]延安大学医学院解剖教研室,陕西省延安市716000 [2]延安市人民医院神经外科,陕西省延安市716000
出 处:《中国组织工程研究》2015年第40期6498-6503,共6页Chinese Journal of Tissue Engineering Research
基 金:陕西省计生委卫生科研项目(2014D30);延安市2013年度科学技术研究发展计划项目(2013-kw33)~~
摘 要:背景:N-甲基-D-天门冬氨酸型受体是与神经突触可塑性密切相关的离子型谷氨酸受体,且由N-甲基-D-天门冬氨酸型受体启动突触的可塑性调节。目的:探索N-甲基-D-天门冬氨酸型受体亚单位N-甲基-D-天门冬氨酸型受体亚单位2A(NR2A)和N-甲基-D-天门冬氨酸型受体亚单位2B(NR2B)在脑缺血后对神经突出的可塑性调节机制。方法:60只Wistar大鼠随机等分为假手术组和脑缺血组,脑缺血组大鼠依据改良型2VO模型方法构建大鼠慢性脑缺血模型,假手术组大鼠不结扎颈总动脉和迷走神经。结果与结论:慢性缺血后0-12 h大鼠大脑海马中NR2A表达水平逐渐降低,而NR2B慢性缺血后4 h达到峰值,且在脑缺血的情况下,无论低频或高频刺激均不能诱导长时程增强的形成。提示NR2B对条件刺激诱导的长时程增强形成有抑制作用;而NR2A对条件刺激长时程增强形成具有促进作用。BACKGROUND: N-methyl-D-aspartate receptor is an ionic glutamate receptor which is closely related with the neural synaptic plasticity, and also can regulate neural synaptic plasticity. OBJECTIVE: To explore the mechanism by which N-methyl-D-aspartate receptor subunits NR2A and NR2B regulate neural synaptic plasticity after cerebral ischemia. METHODS: 60 Wister rats were randomly and evenly divided into a sham-operated group and a cerebral ischemia group. Rat models of chronic cerebral ischemia were established using the modified bilateral common carotid artery occlusion method in the cerebral ischemia group, while rats in the sham-operated group did not undergo occlusion of the common carotid artery and vagus nerve. RESULTS AND CONCLUSION: At 0-12 hours after chronic cerebral ischemia, NR2A expression in the rat hippocampus was gradually decreased, while the expression of NR2B reached its peak level at 4 hours after cerebral ischemia. Under the circumstance of cerebral ischemia, neither low frequency nor high frequency induced long-term potentiation. These findings suggest that NR2B exhibit inhibitory effect, while NR2A exhibit promoting effect on long-term potentiation induced by stimulation.
关 键 词:实验动物 脑及脊髓损伤动物模型 慢性脑缺血 N-甲基-D-天门冬氨酸型受体亚单位2A N-甲基-D-天门冬氨酸型受体亚单位2B 神经突触可塑性 海马CA1区
分 类 号:R318[医药卫生—生物医学工程]
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