[Optic nerve regeneration: contemporary views and perspectives of clinical use]

Recent extensive advances in neuroscience not only proved that optic nerve has a capacity for functional repair, but made its regeneration a reality in laboratory mammals. Today it is evident that optic nerve after axonotmesis displays signs of very active regeneration. Nevertheless, the regeneration is inhibited by a number of factors acting in the environment of normal CNS. Inhibitors secreted by oligodendrocytes and deposited in the layer of myelin attenuate migration of macrophages and process of phagocytosis, which is indispensable for axon regeneration. Astrocytes, which secrete substances supporting nerve regeneration, can not migrate to the injured axons. Glial scar formation prevent axon regrowth and revascularisation. Moreover, immediate expression of certain genes causes axotomised retinal ganglion cells to undergo process of programmed cell death--apoptosis. At present, regeneration of the optic nerve may be successfully promoted in laboratory set-up with substances which can slow down ganglion cells apoptosis and promote axon regrowth. Peripheral nerve bridges and embryonic transplants offer the regenerating axons more friendly environment than that of the normal, matured CNS. One problem, which can not yet be successfully addressed, is how to lead regrowing axons back appropriately to their original targets to reform patterned connections.