The existence of heightened brain plasticity during critical periods in early postnatal life is a central tenet of developmental sensory neuroscience and helps explain the enduring deficits induced by early abnormal sensory exposure [1, 2]. The human visual disorder amblyopia has been linked to unbalanced visual input to the two eyes in early postnatal visual cortical development and has been modeled in animals by depriving them of patterned visual input to one eye [3, 4], a procedure known as monocular deprivation (MD). We investigated the possibility that a period of darkness might reset the central visual pathways to a more plastic stage and hence increase the capacity for recovery from early MD. Here we show that a 10 day period of complete darkness reverses maturation of stable cytoskeleton components in kitten visual cortex and also results in rapid elimination of, or even immunity from, visual deficits linked to amblyogenic rearing by MD. The heightened instability of the cytoskeleton induced by darkness likely represents just one of many parallel molecular changes that promote visual recovery, possibly by release of the various brakes on cortical plasticity [2].
Highlights
► Neurofilament is reduced in kitten visual cortex after a short period of darkness ► Darkness immediately after monocular deprivation prevents development of amblyopia ► Darkness imposed after amblyopia develops results in its disappearance in 5 to 7 days ► Short (10 day) periods of darkness may boost recovery from amblyopia in humans
