Abstract

Our lab has been investigating several factors regulating ocular dominance plasticity in the visual cortex. Our initial work revealed that Chondroitin sulphate proteoglycan (CSPG) removal from the adult visual cortex by means of intracortical infusion of chondroitinase ABC (chABC) activates mechanisms of ocular dominance plasticity in the adult rat visual cortex. These results led to the demonstration that chABC promotes recovery from amblyopia in the adult rat. We have now found that chABC treatment facilitates functional recovery from experimental stroke in adult rats suggesting that regulation of extracellular matrix composition represent a common factor regulating cortical plasticity. CSP Gs are diffusely present in the brain extracellular space but they are also condensed in perineuronal nets. We will discuss recent data showing the involvement in ocular dominance plasticity of specific molecular components of the perineuronal nets and matrix metalloproteases. Plasticity mechanisms also require the activation of intracellular signaling. We previously reported that ERK signaling and histone acetylation (Putignano et al., 2007) are important signaling mechanisms for ocular dominance plasticity. We will discuss these data including new findings showing that pharmacological activation of histone acetylation can promote behavioral recovery from the effects of monocular deprivation in rats.