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The Journal of Neuroscience, November 8, 2006, 26(45):11554-11561; doi:10.1523/JNEUROSCI.3396-06.2006
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Behavioral/Systems/Cognitive
Enhancement of Vision by Monocular Deprivation in Adult Mice
Glen T. Prusky,1 Nazia M. Alam,1 andRobert M. Douglas2 1Department of Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada T1K 3M4, and 2Department of Ophthalmology and Visual Sciences, University of British Columbia, Vancouver, British Columbia, Canada V5Z 3N9
Correspondence should be addressed to Glen T. Prusky at the above address. Email: prusky{at}uleth.ca
Plasticity of vision mediated through binocular interactions has been reported in mammals only during a "critical" period in juvenile life, wherein monocular deprivation (MD) causes an enduring loss of visual acuity (amblyopia) selectively through the deprived eye. Here, we report a different form of interocular plasticity of vision in adult mice in which MD leads to an enhancement of the optokinetic response (OKR) selectively through the nondeprived eye. Over 5 d of MD, the spatial frequency sensitivity of the OKR increased gradually, reaching a plateau of
36% above pre-deprivation baseline. Eye opening initiated a gradual decline, but sensitivity was maintained above pre-deprivation baseline for 5–6 d. Enhanced function was restricted to the monocular visual field, notwithstanding the dependence of the plasticity on binocular interactions. Activity in visual cortex ipsilateral to the deprived eye was necessary for the characteristic induction of the enhancement, and activity in visual cortex contralateral to the deprived eye was necessary for its maintenance after MD. The plasticity also displayed distinct learning-like properties: Active testing experience was required to attain maximal enhancement and for enhancement to persist after MD, and the duration of enhanced sensitivity after MD was extended by increasing the length of MD, and by repeating MD. These data show that the adult mouse visual system maintains a form of experience-dependent plasticity in which the visual cortex can modulate the normal function of subcortical visual pathways.
Key words: optokinetic response; OKR; visual plasticity; learning and memory; ocular dominance; mouse
Received April 6, 2006; revised Sept. 22, 2006; accepted Sept. 22, 2006.
Correspondence should be addressed to Glen T. Prusky at the above address. Email: prusky{at}uleth.ca
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