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Neuro-protective effects of CNTF on hippocampal neurons via an unknown signal transduction pathway
  • ISSN号:0023-074X
  • 期刊名称:《科学通报》
  • 时间:0
  • 分类:R338[医药卫生—人体生理学;医药卫生—基础医学]
  • 作者机构:[1]Department of Psychology, Second Military Medical University, Shanghai 200433, China, [2]Changhai Hospital, Second Military Medical University, Shanghai 200433, China, [3]Laboratory of Stress Medicine, Second Military Medical University, Shanghai 200433, China, [4]School of Basic Medicine, Second Military Medical University, Shanghai 200433,China
  • 相关基金:Acknowledgements We thank Professor He C. from the Department of Neurophysiology of the Second Military Medical University for providing us CNTF reagents and Dr. Norman Fichtenberg from Wayne State University for editing suggestions. This work was supported by the National Natural Science Foundation of China (Grant Nos. 30270364 & 30572080), Medicine and Pharmacy Foundation of PLA (Grant No. 04M021 and "11.5" Special Fund) and Foundation of Second Military Medical University (Grant No. 05JS02).
中文摘要:

在我们的以前的学习,我们建议可以在调停的睫的神经营养的因素(CNTF ) 的已知的信号 transduction 小径的上面的流有一条未知小径 CNTF 的 neuro 保护的函数。在现在的实验,我们观察到在 L-NMDA (在收缩筋的 glutamicacid 离子类型受体) 的非经典的信号 transduction 小径的那 theneuro 保护的功能劝诱了海马趾的神经原损害模型,用主要文化老鼠海马趾的神经原,连续摄影和 gp130 immunohistochemi-cal 试金。结果证明 L-NMDA 导致了海马趾的神经原的有害反应,并且 CNTF 能在海马趾的神经原上禁止 L-NMDA 的有毒的行动。另外,当 CNTF 的 JAK/STATs in the known 经典著作信号 transduction 小径被 PTPi-2 堵住时, CNTF againstL-NMDA 损害的保护的效果仍然存在。L-NMDA 在集中引起了快速的增加海马趾细胞内部免费[Ca~(2+)]_i。 CNTF 能稀释 L-NMDA-induced 举起[Ca~(2+)] _i ,和堵住的 JAK/STATs in the known 经典著作表明 CNTF 的 transduction 小径 affectL-NMDA-induced 举起[Ca~(2+)] _i ,显示那,除了已知的经典著作 signaltransduction 小径,可以有一些另外的 transduction 小径让 CNTF 在海马趾的神经原上施加保护的效果,并且这条小径与有关[Ca~(2+)]。

英文摘要:

In our previous study, we proposed that there may be an unknown pathway in the upper stream of the known signal transduction pathway of Ciliary neurotrophic factor (CNTF) that mediates the neuro-protective function of CNTF. In the present experiment, we observed that the neurorotective function of the non-classic signal transduction pathway in a L-NMDA (a glutamic acid ion type receptor atagonist) induced hippocampal neuron injury model, using primary culture rat hippocampal neurons, continuous photography and gp130 immunohistochemical assay. The results showed that L-NMDA induced injurious reaction of hippocampal neurons, and CNTF was able to inhibit the toxic action of L-NMDA on hippocampal neurons. Additionally, when JAK/STATs in the known classic signal transduction pathway of CNTF were blocked by PTPi-2, the protective effect of CNTF against L-NMDA injury still existed. L-NMDA caused a rapid increase in the concentration of hippocampal intracellular free [Ca^2+]. CNTF was able to attenuate L-NMDA-induced elevation of [Ca^2+], and blocking JAK/STATs in the known classic signal transduction pathway of CNTF did not affect L-NMDA- induced elevation of [Ca^2+], indicating that, apart from the known classic signal transduction pathway, there may be some other transduction pathways for CNTF to exert the protective effect on hippocampal neurons and this pathway is related to [Ca^2+].

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期刊信息
  • 《科学通报》
  • 北大核心期刊(2011版)
  • 主管单位:中国科学院
  • 主办单位:中国科学院
  • 主编:周光召
  • 地址:北京东黄城根北街16号
  • 邮编:100717
  • 邮箱:csb@scichina.org
  • 电话:010-64036120 64012686
  • 国际标准刊号:ISSN:0023-074X
  • 国内统一刊号:ISSN:11-1784/N
  • 邮发代号:80-213
  • 获奖情况:
  • 首届国家期刊奖,中国期刊方阵“双高”期刊,第三届中国出版政府奖
  • 国内外数据库收录:
  • 美国化学文摘(网络版),美国数学评论(网络版),美国工程索引,日本日本科学技术振兴机构数据库,中国中国科技核心期刊,中国北大核心期刊(2004版),中国北大核心期刊(2008版),中国北大核心期刊(2011版),中国北大核心期刊(2014版),中国北大核心期刊(2000版)
  • 被引量:81792