Distinctive features of adult ocular dominance plasticity.
Sensory experience profoundly shapes neural circuitry of juvenile brain. Although the visual cortex of adult rodents retains a capacity for plasticity in response to monocular visual deprivation, the nature of this plasticity and the neural circuit changes that accompany it remain enigmatic. Here, we investigate differences between adult and juvenile ocular dominance plasticity using Fourier optical imaging of intrinsic signals in mouse visual cortex. This comparison reveals that adult plasticity takes longer than in the juvenile mouse, is of smaller magnitude, has a greater contribution from the increase in response to the open eye, and has less effect on the hemisphere ipsilateral to the deprived eye. Binocular deprivation also causes different changes in the adult. Adult plasticity is similar to juvenile plasticity in its dependence on signaling through NMDA receptors. We propose that adult ocular dominance plasticity arises from compensatory mechanisms that counterbalance the loss of afferent activity caused by visual deprivation.
Sato
Masaaki
M
Department of Physiology, W. M. Keck Foundation Center for Integrative Neuroscience, University of California, San Francisco, San Francisco, California 94143-0444, USA.
Stryker
Michael P
MP
D000222:Adaptation, Physiological; D000375:Aging / Q000502:physiology; D000818:Animals; D003423:Critical Period, Psychological; D023882:Dominance, Ocular / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009473:Neuronal Plasticity / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D012683:Sensory Deprivation / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013997:Time Factors; D015348:Vision, Binocular; D015349:Vision, Monocular; D014793:Visual Cortex / Q000502:physiology*
D016194:Receptors, N-Methyl-D-Aspartate