Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation

被引：241

作者：

Heynen, AJ

Yoon, BJ

Liu, CH

Chung, HJ

Huganir, RL

Bear, MF

机构：

[1] MIT, Picower Ctr Learning & Memory, Howard Hughes Med Inst, Cambridge, MA 02139 USA

[2] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA

[3] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA

[4] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

来源：

NATURE NEUROSCIENCE | 2003年 / 6卷 / 08期

关键词：

D O I：

10.1038/nn1100

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

A dramatic form of experience-dependent synaptic plasticity is revealed in visual cortex when one eye is temporarily deprived of vision during early postnatal life. Monocular deprivation (MD) alters synaptic transmission such that cortical neurons cease to respond to stimulation of the deprived eye, but how this occurs is poorly understood. Here we show in rat visual cortex that brief MD sets in motion the same molecular and functional changes as the experimental model of homosynaptic long-term depression (LTD), and that prior synaptic depression by MD occludes subsequent induction of LTD. The mechanisms of LTD, about which there is now a detailed understanding, therefore contribute to visual cortical plasticity.

引用

页码：854 / 862

页数：9

共 51 条

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