Activation of RHO GTPase triggers structural remodelling and functional plasticity in the adult rat visual cortex

Experience-dependent cortical plasticity is maximal during early life and decreases thereafter. Dendritic spines undergo remodelling in juvenile age but are far more stable in adulthood. Here we have tested whether this reduction in dendritic spine dynamics sets the limit for experience-dependent plasticity in adult age. Injection of a bacterial toxin, CNF1, into the adult rat visual cortex triggered a long-lasting activation of the Rho GTPase Rac1, with a consequent increase in spine density and length in pyramidal neurons. Adult rats treated with CNF1, but not controls, showed an ocular dominance (OD) shift towards the open eye following monocular deprivation. CNF1-mediated OD plasticity was selectively due to a potentiation of open eye responses. Thus, CNF1 sets in motion a mechanism of activity-dependent takeover by which newly formed dendritic sites are contacted preferentially by more active afferents from the open eye. The plasticizing effect of Rho GTPase activation may be exploited to promote brain repair.