A study of monocular deprivation (MD) in rats reveals an enhancement of visual acuity through the non-deprived eye after long periods of MD. Moreover, a subsequent period of eye opening and reclosing suggests that there is a considerable plasticity of visual function into adulthood.

Brief periods of MD, or MD commenced in adulthood, typically have no long-term effects on visual function. However, if MD is commenced during early postnatal life and prolonged into adulthood there are pronounced effects on the function of the visual cortex, with most visual cortex neurons no longer being excited by input to the deprived eye, but only by input to the non-deprived eye. Unsurprisingly, this change is accompanied by an impairment of visually guided behaviour through the deprived eye. Recently, electrophysiological recordings of the mouse visual cortex showed that MD results not only in a depression of visually evoked potentials through the deprived eye, but also an enhancement of visually evoked potentials through the non-deprived eye. However, it was uncertain whether the latter effect was associated with a change in visual function in the non-deprived eye.

Mark Bear and colleagues assessed the behavioural significance of these findings by measuring visual acuity in rats after five months of MD that began at postnatal day 21. As expected, MD resulted in a decrease in visual acuity through the deprived eye; in addition, however, MD also produced an enhancement of visual acuity over and above normal levels through the non-deprived eye. This suggests that the previously described changes in visually evoked potentials following MD are functionally relevant.

Following the opening of the deprived eye, and restoration of binocular vision, there was a reduction to near-normal levels of visual acuity through the non-deprived eye, which was followed by a gradual but incomplete recovery of acuity through the deprived eye. To determine whether this plasticity of visual function was reversible and preserved in adulthood, animals were then subjected to a second period of MD. Visual acuity through the non-deprived eye increased once more to the same enhanced level seen after the initial period of MD. When binocular vision was again restored, acuity through the non-deprived eye declined once more, whereas acuity through the deprived eye, which had decreased during the period of MD, recovered with time.

These findings show a robust and reversible plasticity in the visual function of rats that extends well into adulthood. It will be interesting to elucidate the physiological and molecular mechanisms responsible for these changes in visual performance and how these might contribute to enhanced vision or 'lazy eye' syndrome in humans.