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趋化因子 MCP-1对大鼠海马区NMDA受体介导的兴奋性突触后电流的影响

李珊 胡喆 周燕 熊焕贵

中国药理学通报2016,Vol.32Issue(7):950-955,6.
中国药理学通报2016,Vol.32Issue(7):950-955,6.DOI:10.3969/j.issn.1001-1978.2016.07.013

趋化因子 MCP-1对大鼠海马区NMDA受体介导的兴奋性突触后电流的影响

Effects of chemokine MCP-1 on NMDA-mediated exciatory postsynaptic current in hippocampal slice of rats

李珊 1胡喆 1周燕 1熊焕贵2

作者信息

  • 1. 广西医科大学药学院,广西南宁 530021
  • 2. 美国内布拉斯加州立大学医学中心神经科学与药理学系,美国奥马哈 NE68198-5880
  • 折叠

摘要

Abstract

Aim To explore how MCP-1 induces neu-rodisorder by determing the effects of MCP-1 on excita-tory postsynaptic current(EPSCs) in the CA1 region of rat hippocampal brain slices .Methods EPSCs, the AMPA receptor-mediated EPSC (EPSCAMPAR ), NMDA receptor mediated EPSCs(EPSCNMDAR) and NR2BR re-ceptor-mediated EPSC ( EPSCNR2BR ) were recorded u-sing whole-cell patch recording techniques to observe the effects of 2.3 nmol· L-1 MCP-1 on pyramidal neu-rons in hippocampal CA1 region.Microtubule-associat-ed protein-2 ( MAP-2 ) staining was used to study whether MCP-1 induced dendritic injuries in hippocam-pal CA1 region and whether NMDAR , AMPAR or CCR2 receptor antagonists had protective effects a-gainst dendritic damage caused by MCP-1.Results ① Bath application of MCP-1 produced a significant enhancement of the amplitudes of EPSCs , EPSCAMPAR and EPSCNMDAR .②Further studies revealed that MCP-1 potentiated EPSC NR2BR; ③ The MCP-1-associated dendritic injuries were blocked by NMDAR , AMPAR and CCR2R antagonists respectively .Conclusions Our results suggest a potential role of MCP-1 which may play in neuroexcitotoxicity and neural injury via NMDA receptor(especially NMDAR subtype NR2BR) and CCR2 receptor .The antagonists of these receptors may have potential therapeutic effect for neurodegener-ation.

关键词

趋化因子/MCP-1/海马脑片/兴奋性突触后电流/神经兴奋性毒性/艾滋性认知功能障碍

Key words

chemokine/MCP-1/hippocampal slices/EPSCs/neuroexcitoxicity/HAND

分类

医药卫生

引用本文复制引用

李珊,胡喆,周燕,熊焕贵..趋化因子 MCP-1对大鼠海马区NMDA受体介导的兴奋性突触后电流的影响[J].中国药理学通报,2016,32(7):950-955,6.

基金项目

国家自然科学基金课题( No 81360192);广西自然科学基金(No 2012GXNSFCA053004);广西教育厅高等学校资助科研项目 ()

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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