PRESENCE OF GROWTH-INHIBITORS IN FISH OPTIC-NERVE MYELIN - POSTINJURYCHANGES

This study shows that the fish optic nerve, which is able to regenerat e after injury, contains myelin-associated growth inhibitors similar t o the growth inhibitors present in mammalian central nervous system (C NS) myelin. The ability of nerves to regenerate was previously correla ted with the ability of sections from these nerves to support neuronal attachment and axonal growth in vitro. Thus neuroblastoma cells or em bryonic neurons became attached to and grew axons on sections of rat s ciatic nerve or fish optic nerve, which are spontaneously regenerating systems, but not on sections of rat optic nerve, a nonregenerating sy stem. Failure of the latter to support axonal growth has been attribut ed, at least in part, to growth inhibitors. Recently it was shown that adult neurons, which differ in their growth requirement from embryoni c neurons, are unable to extend neurites on sections of normal sciatic nerve but are able to extend neurites on sections of sciatic nerve th at was injured prior to its excision. We found a similar situation in the fish optic nerve, i.e., that the nerve is normally not permissive to growth of adult retinal axons but becomes growth permissive after i njury. The nonpermissiveness of the normal fish optic nerve was found to correlate with the presence of myelin-associated growth-inhibitory molecules. This inhibitory activity of fish myelin was neutralized by IN-1 antibodies, known to neutralize rat myelin growth inhibitors. The results thus demonstrate that fish optic nerve myelin contains inhibi tors apparently similar or even identical to those of rat, but possibl y present in lower amounts than in the rat. Results are discussed with respect to the possibility that fish optic nerve, like the rat sciati c nerve and unlike the rat optic nerve, undergoes certain changes afte r injury that support regeneration of adult neurons. Such changes migh t include elimination or neutralization of growth inhibitors. (C) 1994 Wiley-Liss, Inc.