...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Neurophysiology >Activation of postsynaptic Ca2+ stores modulates glutamate receptor cycling in hippocampal neurons.
【24h】

Activation of postsynaptic Ca2+ stores modulates glutamate receptor cycling in hippocampal neurons.

机译：突触后钙离子存储的激活调节海马神经元中的谷氨酸受体循环。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We show that activation of postsynaptic inositol 1,4,5-tris-phosphate receptors (IP(3)Rs) with the IP(3)R agonist adenophostin A (AdA) produces large increases in AMPA receptor (AMPAR) excitatory postsynaptic current (EPSC) amplitudes at hippocampal CA1 synapses. Co-perfusion of the Ca(2+) chelator bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid strongly inhibited AdA-enhanced increases in EPSC amplitudes. We examined the role of AMPAR insertion/anchoring in basal synaptic transmission. Perfusion of an inhibitor of synaptotagmin-soluble n-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor SNARE-mediated exocytosis depressed basal EPSC amplitudes, whereas a peptide that inhibits GluR2/3 interactions with postsynaptic density-95 (PDZ) domain proteins glutamate receptor interacting protein (GRIP)/protein interacting with C-kinase-1 (PICK1) enhanced basal synaptic transmission. These results suggest that constitutive trafficking and anchoring of AMPARs help maintain basal synaptic transmission. The regulation of postsynaptic AMPAR trafficking involves synaptotagmin-SNARE-mediated vesicle exocytosis and interactions between AMPARs and the PDZ domains in GRIP/PICK1. We show that inhibitors of synaptotagmin-SNARE-mediated exocytosis, or interactions between AMPARs and GRIP/PICK1, attenuated AdA-enhanced increases in EPSC amplitudes. These results suggest that IP(3)R-mediated Ca(2+) release can enhance AMPAR EPSC amplitudes through mechanisms that involve AMPAR-PDZ interactions and/or synaptotagmin-SNARE-mediated receptor trafficking.
机译：我们显示，与IP（3）R激动剂腺苷A（AdA）的突触后肌醇1,4,5-三磷酸受体（IP（3）Rs）的激活在AMPA受体（AMPAR）兴奋性突触后电流（海马CA1突触的振幅。 Ca（2+）螯合剂双-（邻氨基苯氧基）-N，N，N'，N'-四乙酸的共灌注强烈抑制AdA增强的EPSC幅度增加。我们研究了AMPAR插入/锚定在基础突触传递中的作用。灌注突触素可溶性n-乙基马来酰亚胺敏感因子附着蛋白（SNAP）抑制剂的抑制剂SNARE介导的胞吐作用降低了基础EPSC幅度，而抑制GluR2 / 3与突触后密度95（PDZ）域蛋白谷氨酸受体相互作用的肽相互作用蛋白（GRIP）/与C激酶-1（PICK1）相互作用的蛋白增强了基础突触传递。这些结果表明，AMPAR的组成型运输和锚定有助于维持基础突触传递。突触后AMPAR转运的调控涉及突触小蛋白-SNARE介导的囊泡胞吐作用以及GRIP / PICK1中AMPAR与PDZ域之间的相互作用。我们显示，突触素-SNARE介导的胞吐作用或AMPAR与GRIP / PICK1之间的相互作用的抑制剂减弱了AdA增强的EPSC振幅。这些结果表明IP（3）R介导的Ca（2+）释放可以通过涉及AMPAR-PDZ相互作用和/或突触小蛋白-SNARE介导的受体运输的机制来增强AMPAR EPSC振幅。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号