• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Nature >Postsynaptic synaptotagmins mediate AMPA receptor exocytosis during LTP
【24h】

Postsynaptic synaptotagmins mediate AMPA receptor exocytosis during LTP

机译：突触后突触素介导LTP期间AMPA受体胞吐作用

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

Strengthening of synaptic connections by NMDA (N-methyl-d-aspartate) receptor-dependent long-term potentiation (LTP) shapes neural circuits and mediates learning and memory. During the induction of NMDA-receptor-dependent LTP, Ca2+ influx stimulates recruitment of synaptic AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors, thereby strengthening synapses. How Ca2+ induces the recruitment of AMPA receptors remains unclear. Here we show that, in the pyramidal neurons of the hippocampal CA1 region in mice, blocking postsynaptic expression of both synaptotagmin-1 (Syt1) and synaptotagmin-7 (Syt7), but not of either alone, abolished LTP. LTP was restored by expression of wild-type Syt7 but not of a Ca2+-binding-deficient mutant Syt7. Blocking postsynaptic expression of Syt1 and Syt7 did not impair basal synaptic transmission, reduce levels of synaptic or extrasynaptic AMPA receptors, or alter other AMPA receptor trafficking events. Moreover, expression of dominant-negative mutant Syt1 which inhibits Ca2+-dependent presynaptic vesicle exocytosis, also blocked Ca2+-dependent postsynaptic AMPA receptor exocytosis, thereby abolishing LTP. Our results suggest that postsynaptic Syt1 and Syt7 act as redundant Ca2+-sensors for Ca2+-dependent exocytosis of AMPA receptors during LTP, and thereby delineate a simple mechanism for the recruitment of AMPA receptors that mediates LTP.
机译：NMDA（N-甲基-d-天冬氨酸）受体依赖的长期增强（LTP）增强突触连接可塑造神经回路并介导学习和记忆。在诱导NMDA受体依赖性LTP的过程中，Ca2 +涌入会刺激突触AMPA（α-氨基-3-羟基-5-甲基-5-甲基-4-异恶唑丙酸）受体的募集，从而增强突触。 Ca 2+如何诱导AMPA受体募集尚不清楚。在这里，我们显示，在小鼠海马CA1区的锥体神经元中，阻断synaptotagmin-1（Syt1）和synaptotagmin-7（Syt7）的突触后表达，但不能单独消除LTP。 LTP通过野生型Syt7的表达恢复，但不表达Ca2 +结合缺陷型突变Syt7。阻断Syt1和Syt7的突触后表达不会损害基础突触传递，降低突触或突触外AMPA受体的水平或改变其他AMPA受体的转运事件。此外，抑制Ca2 +依赖的突触前囊泡胞吐作用的显性负突变Syt1的表达，也阻断了Ca2 +依赖的突触后AMPA受体胞吐作用，从而废除了LTP。我们的结果表明，突触后Syt1和Syt7充当LTP期间AMPA受体的Ca2 +依赖性胞吐作用的冗余Ca2 +传感器，从而描绘出了介导LTP的AMPA受体募集的简单机制。

著录项

  • 来源
    《Nature》 |2017年第7650期|316-321|共6页
  • 作者

    Wu Dick; Bacaj Taulant; Morishita Wade; Goswami Debanjan; Arendt Kristin L.; Xu Wei; Chen Lu; Malenka Robert C.; Sudhof Thomas C.;

  • 作者单位

    Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Nancy Pritzker Lab, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Nancy Pritzker Lab, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Nancy Pritzker Lab, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA|UT Southwestern Med Ctr, Dept Neurosci, Dallas, TX 75235 USA;

    Stanford Univ, Sch Med, Dept Neurosurg, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Nancy Pritzker Lab, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA;

    Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA|Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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