RETINAL AXON REGENERATION IN THE LIZARD GALLOTIA-GALLOTI IN THE PRESENCE OF CNS MYELIN AND OLIGODENDROCYTES

Retinal ganglion cell (RGC) axons in lizards (reptiles) were found to regenerate after optic nerve injury. To determine whether regeneration occurs because the visual pathway has growth-supporting glia cells or whether RGC axons regrow despite the presence of neurite growth-inhib itory components, the substrate properties of lizard optic nerve myeli n and of oligodendrocytes were analyzed in vitro, using rat dorsal roo t ganglion (DRG) neurons. In addition, the response of lizard RGC axon s upon contact with rat and reptilian oligodendrocytes or with myelin proteins from the mammalian central nervous system (CNS) was monitored . Lizard optic nerve myelin inhibited extension of rat DRG neurites, a nd lizard oligodendrocytes elicited DRG; growth cone collapse. Both ef fects were partially reversed by antibody IN-1 against mammalian 35/25 0 kD neurite growth inhibitors, and IN-1 stained myelinated fiber trac ts in the lizard CNS. However, lizard RGC growth cones grew freely acr oss oligodendrocytes from the rat and the reptilian CNS. Mammalian CNS myelin proteins reconstituted into liposomes and added to elongating lizard RGC axons caused at most a transient collapse reaction. Growth cones always recovered within an hour and regrew. Thus, lizard CNS mye lin and oligodendrocytes possess nonpermissive substrate properties fo r DRG neurons-like corresponding structures and cells in the mammalian CNS, including mammalian-like neurite growth inhibitors. Lizard RGC a xons, however, appear to be far less sensitive to these inhibitory sub strate components and therefore may be able to regenerate through the visual pathway despite the presence of myelin and oligodendrocytes tha t block growth of DRG neurites. (C) 1998 Wiley-Liss, Inc.