• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文OA文献 >Experience-dependent plasticity without long-term depression by type 2 metabotropic glutamate receptors in developing visual cortex
【2h】

Experience-dependent plasticity without long-term depression by type 2 metabotropic glutamate receptors in developing visual cortex

机译：2型代谢型谷氨酸受体在视觉皮层发育过程中没有长期抑制的经验依赖性可塑性

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Synaptic depression is thought to underlie the loss of cortical responsiveness to an eye deprived of vision. Here, we establish a fundamental role for type 2 metabotropic glutamate receptors (mGluR2) in long-term depression (LTD) of synaptic transmission within primary visual cortex. Direct mGluR2 activation by (2S,2′R,3′R-2-(2′,3′-dicarboxycyclopropyl)glycine (DCG-IV) persistently depressed layer 2/3 field potentials in slices of mouse binocular zone when stimulated concomitantly. Chemical LTD was independent of N-methyl-d-aspartate (NMDA) receptors but occluded conventional LTD by low-frequency stimulation, indicating shared downstream events. Antagonists or targeted disruption of mGluR2 conversely prevented LTD induction by electrical low-frequency stimulation to layer 4. In contrast, Schaeffer collateral synapses did not exhibit chemical LTD, revealing hippocampal area CA1, naturally devoid of mGluR2, to be an inappropriate model for neocortical plasticity. Moreover, monocular deprivation remained effective in mice lacking mGluR2, and receptor expression levels were unchanged during the critical period in wild-type mice, indicating that experience-dependent plasticity is independent of LTD induction in visual cortex. Short-term depression that was unaffected by mGluR2 deletion may better reflect circuit refinement in vivo.
机译：突触性抑郁被认为是丧失视力的眼睛皮质反应能力丧失的基础。在这里，我们建立了2型代谢型谷氨酸受体（mGluR2）在初级视觉皮层内的突触传递的长期抑制（LTD）的基本作用。 （2S，2'R，3'R-2-（2'，3'-二羧基环丙基）甘氨酸（DCG-IV）的直接mGluR2激活在相伴刺激下会持续抑制小鼠双眼区切片中的2/3层电势。 Chemical LTD独立于N-甲基-d-天冬氨酸（NMDA）受体，但通过低频刺激封闭了常规LTD，表明共有下游事件发生；拮抗药或mGluR2的定向破坏反过来阻止了低频电刺激第4层的LTD诱导。相比之下，Schaeffer侧突触未显示化学LTD，揭示了自然缺乏mGluR2的海马区CA1是新皮层可塑性的不适当模型；此外，单眼剥夺在缺乏mGluR2的小鼠中仍然有效，并且受体表达水平在此期间没有变化。在野生型小鼠的关键时期，这表明经验依赖的可塑性独立于视皮层中的LTD诱导。 mGluR2缺失可能更好地反映体内电路的细化。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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