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代谢型谷氨酸受体信号传导对于视觉皮层中NMDA受体依赖性眼优势可塑性和长时程抑制是必需的。

Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex.

作者信息

Sidorov Michael S, Kaplan Eitan S, Osterweil Emily K, Lindemann Lothar, Bear Mark F

机构信息

The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139.

The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139

出版信息

Proc Natl Acad Sci U S A. 2015 Oct 13;112(41):12852-7. doi: 10.1073/pnas.1512878112. Epub 2015 Sep 28.

Abstract

A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.

摘要

出生后早期新皮层发育的一个特征是通过代谢型谷氨酸受体5(mGluR5)的信号传导出现短暂峰值。在视觉皮层中,这种变化与兴奋性突触对单眼剥夺(MD)的敏感性增加相吻合。然而,MD后视觉反应性的丧失是通过对突触传递的长时程抑制(LTD)研究揭示的机制发生的,在第4层中,这是由NMDA受体(NMDARs)而非mGluR5的急性激活诱导的。我们在此报告,出生后慢性下调mGluR5信号传导会在体外NMDAR依赖性LTD和体内眼优势可塑性方面产生协调性损伤。数据表明,出生后发育关键期持续的mGluR5信号传导建立了生化条件,这些条件允许通过NMDAR依赖性LTD机制对兴奋性突触进行活动依赖性塑造。

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