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

Arnold J. Heynen, Bongjune Yoon, Cheng Hang Liu, Hee J. Chung, Richard L. Huganir, Mark F. Bear

Research output: Contribution to journalArticle

238 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)854-862
Number of pages9
JournalNature Neuroscience
Volume6
Issue number8
DOIs
Publication statusPublished - 2003 Aug 1
Externally publishedYes

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Visual Cortex
Long-Term Synaptic Depression
Depression
Neuronal Plasticity
Synaptic Transmission
Theoretical Models
Neurons

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation. / Heynen, Arnold J.; Yoon, Bongjune; Liu, Cheng Hang; Chung, Hee J.; Huganir, Richard L.; Bear, Mark F.

In: Nature Neuroscience, Vol. 6, No. 8, 01.08.2003, p. 854-862.

Research output: Contribution to journalArticle

Heynen, Arnold J. ; Yoon, Bongjune ; Liu, Cheng Hang ; Chung, Hee J. ; Huganir, Richard L. ; Bear, Mark F. / Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation. In: Nature Neuroscience. 2003 ; Vol. 6, No. 8. pp. 854-862.
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