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β1整合素抑制β淀粉样蛋白对记忆长时程增强的作用
引用本文:韩海燕,张逸驰,季淑琼,梁奇明,朱遂强,薛峥. β1整合素抑制β淀粉样蛋白对记忆长时程增强的作用[J]. 中国临床康复, 2013, 0(11): 1959-1964
作者姓名:韩海燕  张逸驰  季淑琼  梁奇明  朱遂强  薛峥
作者单位:[1]华中科技大学同济医学院附属同济医院神经内科,湖北省武汉市430030 [2]首都医科大学宣武医院神经内科,北京市100053
基金项目:课题由国家自然科学基金(30700244)资助.
摘    要:
背景:抑制小鼠海马脑片整合素活动后,虽然不会影响长时程增强的诱导,但却带来快速的长时程增强衰减,证明整合素对于诱导后长时程增强的维持和稳定起到关键的作用。目的:通过在体电生理技术阐明整合素的β1亚基在活体大鼠的海马CA1区中β淀粉样蛋白抑制长时程增强的过程中所起到的作用。方法:将15只SD大鼠等分为对照组、G淀粉样蛋白组和β1整合素拮抗剂组,分别给予生理盐水,β淀粉样蛋白和β1整合素的选择性拮抗剂,记录自给予β淀粉样蛋白前10min至高频强直刺激后3h时的兴奋性突触后电位。结果与结论:给予对照组大鼠高频强刺激后兴奋性突触后电位明显增强,增幅在30%以上。β淀粉样蛋白组大鼠给予高频强刺激后兴奋性突触后电位在3h中被显著抑制,没有出现明显的变化。而β1整合索拈抗剂组大鼠给予高频强刺激后兴奋性突触后电位又出现明显的增强。推测β1整合素在活体大鼠的海马CA1区中β淀粉样蛋白抑制长时程增强的过程中可能起着重要的介导作用,而其特异性的拮抗剂或抗体可以阻断这种介导作用。

关 键 词:组织构建  组织构建与生物活性因子  阿尔茨海默病  神经毒性  β淀粉样蛋白  长时程增强  β1整合素亚基  海马CA1区  高频刺激  兴奋性突触后电位  国家自然科学基金  组织构建图片文章

ntegrin beta 1 inhibits long-term potentiation nduced by amyloid beta-protein
Han Hai-yan,Zhang Yi-chi,Ji Shu-qiong,Liang Qi-ming,Zhu Sui-qiang,Xue Zheng. ntegrin beta 1 inhibits long-term potentiation nduced by amyloid beta-protein[J]. Chinese Journal of Clinical Rehabilitation, 2013, 0(11): 1959-1964
Authors:Han Hai-yan  Zhang Yi-chi  Ji Shu-qiong  Liang Qi-ming  Zhu Sui-qiang  Xue Zheng
Affiliation:1 Department of Neurology Province, China 2 Department of Neurology Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei Xuanwu Hospital, Capital Medical University, Beijing 100053, China)
Abstract:
BACKGROUND: Inhibition of integrin activity in the hippocampal slices of mice cannot influence the induction of long-term potentiation, but bring rapid long-term potentiation attenuation, proving integrin plays a key role in maintaining and stabilizing the long-term potentiation after induction. OBJECTIVE: To explain the influence of integrin beta-1 subunit during the inhibition of long-term potentiation induced by amyloid beta-protein in rat hippocampus CA1 in vivo using electrophysiological technology. METHODS: Fifteen Sprague-Dawley rats were equally randomized into control group treated with normal saline, amyloid beta-protein group treated with amyloid beta-protein, and integrin beta-1 subunit inhibitor group treated with selective antagonist for integrin beta-1 subunit. Excitatory postsynaptic potentials were recorded from 10 minutes before amyloid beta-protein administration till 3 hours after high-frequency tetanic stimulation. RESULTS AND CONCLUSION: In the control group, excitatory postsynaptic potentials were enhanced significantly with an increment of 30%. In the amyloid beta-protein group, excitatory postsynaptic potentials were obviously restraint within 3 hours after high-frequency tetanic stimulation and had no remarkable increase. It can be speculated by the results that integrin beta-1 subunit may be important to the long-term potentiation inhibited by amyloid beta-protein in the rat hippocampal CA1 region in vivo. The special inhibitor or antibody of integrin beta-1 subunit has the ability to stop the mediation.
Keywords:tissue construction  tissue construction and bioactive factors  Alzheimer's disease  neurotoxicity  amyloid beta-protein  long-term potentiation  integrin beta-1 subunit  hippocampal CA1 region  high-frequency stimulation  excitatory postsynaptic potential  the National Natural Science Foundation of China  tissue construction photographs-containing paper
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