Nature Neuroscience6, 854 - 862 (2003)
Published online: 28 July 2003; | doi:10.1038/nn1100
Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation
Arnold J Heynen1, 3, Bong-June Yoon1, 3, Cheng-Hang Liu1, Hee J Chung2, Richard L Huganir2
& Mark F Bear1
1
Howard Hughes Medical Institute, The Picower Center for Learning and Memory, and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.
2
Howard Hughes Medical Institute and Department of Neuroscience, Johns Hopkins University Medical School, Baltimore, Maryland 21205, USA.
3
These authors contributed equally to this work.
Correspondence should be addressed to Mark F Bear mbear@mit.edu
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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