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The Journal of Neuroscience, March 15, 2006, 26(11):2951-2955; doi:10.1523/JNEUROSCI.5554-05.2006

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Brief Communications
Visual Deprivation Reactivates Rapid Ocular Dominance Plasticity in Adult Visual Cortex

Hai-Yan He,2 William Hodos,1,3 and Elizabeth M. Quinlan1,2

1Neuroscience and Cognitive Sciences Program and Departments of 2Biology and 3Psychology, University of Maryland, College Park, Maryland 20742

Correspondence should be addressed to Elizabeth M. Quinlan, 3245 Biology/Psychology Building #144, University of Maryland, College Park, MD 20742. Email: equinlan{at}umd.edu

Brief monocular deprivation (≤3 d) induces a rapid shift in the ocular dominance of binocular neurons in the juvenile rodent visual cortex but is ineffective in adults. Here, we report that persistent, rapid, juvenile-like ocular dominance plasticity can be reactivated in adult rodent visual cortex when monocular deprivation is preceded by visual deprivation. Ocular dominance shifts in visually deprived adults are caused by a rapid depression of the response to stimulation of the deprived eye, previously only reported in juveniles, and a simultaneous potentiation of the response to stimulation of the nondeprived eye. The enhanced ocular dominance plasticity induced by visual deprivation persists for days, even if binocular vision precedes monocular deprivation. Visual deprivation also induces a significant decrease in the level of GABAA receptors relative to AMPA receptors and a return to the juvenile form of NMDA receptors in the visual cortex, two molecular changes that we propose enable the persistent reactivation of rapid ocular dominance plasticity.

Key words: visual deprivation; ocular dominance; AMPA receptor; NMDA receptor; GABAA receptor; synaptic plasticity


Received Dec. 27, 2005; revised Jan. 30, 2006; accepted Feb. 2, 2006.

Correspondence should be addressed to Elizabeth M. Quinlan, 3245 Biology/Psychology Building #144, University of Maryland, College Park, MD 20742. Email: equinlan{at}umd.edu




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