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

Arnold J. Heynen; Bong June Yoon; Cheng Hang Liu; Hee J. Chung; Richard L. Huganir; Mark F. Bear

doi:10.1038/nn1100

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

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

Research output: Contribution to journal › Article › peer-review

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 language	English (US)
Pages (from-to)	854-862
Number of pages	9
Journal	Nature Neuroscience
Volume	6
Issue number	8
DOIs	https://doi.org/10.1038/nn1100
State	Published - Aug 1 2003
Externally published	Yes

ASJC Scopus subject areas

Neuroscience(all)

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10.1038/nn1100

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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.",

author = "Heynen, {Arnold J.} and Yoon, {Bong June} and Liu, {Cheng Hang} and Chung, {Hee J.} and Huganir, {Richard L.} and Bear, {Mark F.}",

note = "Funding Information: We thank C. Orsini from the laboratory of L. Maffei (Pisa, Italy) for providing VEP software, and E. Sklar, K. Clayton, K. Miller and S. Meagher for assistance. The work was funded by the Howard Hughes Medical Institute and the National Eye Institute.",

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AU - Heynen, Arnold J.

AU - Yoon, Bong June

AU - Liu, Cheng Hang

AU - Chung, Hee J.

AU - Huganir, Richard L.

AU - Bear, Mark F.

N1 - Funding Information: We thank C. Orsini from the laboratory of L. Maffei (Pisa, Italy) for providing VEP software, and E. Sklar, K. Clayton, K. Miller and S. Meagher for assistance. The work was funded by the Howard Hughes Medical Institute and the National Eye Institute.

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N2 - 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.

AB - 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.

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

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