Esperienza, plasticità, riparazione del danno e recupero della funzione nervosa

Repair of brain damage induced by traumatic, vascular or degenerative injury depends on the ability of neurons to regenerate their axons or to reorganize spared circuits so to restore function . In the adult mammalian central nervous system regenerative processes are hampered by a set of molecules that actively inhibit neuritic elongation . Such factors are present in the intact nervous tissue, where they regulate physiological plasticity to maintain specific connection patterns . Neutralization of inhibitory mechanisms promotes neuritic elongation, but it is not sufficient to establish, or re- establish, functionally meaningful synaptic contacts . On the other hand, interaction with the external world favours plasticity by modulating regulatory mechanisms . Therefore, the outcome of brain repair depends on the triadic interaction between intrinsic neuronal properties, regulatory molecules in the nervous tissue and the external world . Molecular interactions between neurons and the surrounding microenvironment exert a primarily permissive function on neuritic growth, whereas external stimuli play an essential instructive role on the arrangement of newly-formed contacts . Hence, efficient therapeutic strategies for brain damage require the combination of specific molecular manipulations and targeted rehabilitation paradigms