Cross‐modal restoration of ocular dominance plasticity in adult mice

The temporal closure of one eye in juvenile and young adult mice induces a shift of the ocular dominance (OD) of neurons in the binocular visual cortex. However, OD plasticity typically declines with age and is completely absent in matured mice beyond postnatal day (PD) 110. As it has been shown that the deprivation of one sensory input can induce neuronal alterations in non‐deprived sensory cortices, we here investigated whether cross‐modal interactions have the potential to reinstall OD plasticity in matured mice. Strikingly, using intrinsic signal imaging we could demonstrate that both whisker deprivation and auditory deprivation for only one week reinstated OD plasticity in fully adult mice. These OD shifts were always mediated by an increase of V1 responsiveness to visual stimulation of the open eye, a characteristic feature of OD plasticity normally only found in young adult mice. Moreover, systemic administration of the competitive NMDA receptor antagonist CPP completely abolished cross‐modally induced OD plasticity. Taken together, we demonstrate here for the first time that the deprivation of non‐visual senses has the potential to rejuvenate the adult visual cortex. The temporal closure of one eye in young mice provokes a shift of the ocular dominance of neurons in the visual cortex. However, this type of plasticity is completely absent in fully adult mice. In this study, Teichert et al. demonstrate that a deprivation of a non‐visual sense (somatosensory or auditory) can cross‐modally restore visual cortex plasticity in fully adult mice. These results demonstrate the massive potential of cross‐modal plasticity in the adult brain.