Abstract
We have recently shown that the adult visual cortex retains a degree of neuroplasticity higher than previously thought by demonstrating that short-term monocular deprivation unexpectedly boosts the deprived eye (measured as increased predominance in binocular rivalry) and that this form of plasticity is mediated by a decrease in GABA concentration in the visual cortex (Lunghi et al, 2011, 2015). Recent studies using animal models have shown that physical exercise promotes visual plasticity by altering the excitation/inhibition balance in the primary visual cortex. We hypothesized that physical activity could enhance visual plasticity also in humans. To test this hypothesis we measured binocular rivalry between orthogonal luminance-modulated gratings (size 2°, spatial frequency: 2 cpd, contrast: 50%) in 20 adult volunteers before and after 2 hours of monocular deprivation in two conditions: an inactive control condition in which, during the deprivation period, subjects watched a movie while sitting on a chair, and a physical activity condition in which, during the deprivation period, subjects watched a movie while intermittently cycling on a stationary bicycle. We found that in the physical activity condition the effect of deprivation on binocular rivalry was potently enhanced compared to the inactive control condition: the deprived eye predominance in binocular rivalry was higher compared to the inactive control condition for at least 120 minutes after eye-patch removal. These results demonstrate that moderate levels of physical activity enhance short-term plasticity of the adult visual cortex by boosting the homeostatic response of the visual system to transient monocular deprivation, probably by inducing a change in the primary visual cortex excitation/inhibition balance. Enhancing neuroplasticity in adult subjects is fundamental for the treatment of amblyopia, that is thought to be untreatable in adulthood and for a number of different conditions, such as recovery after brain injury and prevention of pathological brain aging.
Meeting abstract presented at VSS 2016