Neuronal Nogo‐A in New‐born Retinal Ganglion Cells: Implication for the Formation of the Age‐related Fiber Order in the Optic Tract

Abstract

Nogo-A is highly expressed in oligodendrocytes in the adult central nervous system (CNS). Recently it was found that Nogo-A is also expressed in some neuronal types during development. Here, we examined the expression pattern of Nogo-A in both the retina and optic tract (OT) of mouse embryos from E12 to E15. After perturbation of its function in the OT for 5 hr in the brain slice culture system using a Nogo-A specific antibody or antagonist of its receptor (NEP1-40), the optic nerve fibers and growth cones were traced with DiI. We showed that most Tuj-1 positive new-born neurons at E12 were Nogo-A positive. At E15, retinal neurons reduced the Nogo-A expression. It was worth noting that some projecting axons expressed Nogo-A along the retinofugal pathway. On the basis of their specific locations within the superficial half of the OT and the colocalization with GAP-43 (a marker for the newly born growth cones and axons), we concluded that those Nogo-A positive axons were the newly arrived retinal fibers. Blocking the function of Nogo-A with Nogo-A antibody or NEP1-40 resulted in the shift of DiI labeled axons and growth cones from the superficial half to the whole depth of the OT. These results indicate that Nogo-A in the newly born retinal ganglion cells (RGCs) and their axons are involved in sorting out the newly arrived axons to the subpial region of the OT. Anat Rec, 299:1027Rec, 299: -1036Rec, 299: , 2016. V C 2016 Wiley Periodicals, Inc.Key words: Nogo-A; RGCs; axon guidance; optic tract; mouse embryoAxon outgrowth and pathfinding are important aspects of neural development. The RGCs, which are the only neuronal type which send axons out of the eye to connect with targets in the brain, provide a good model to study axon guidance and pathfinding. During the development of the visual pathway, various retinofugal projections are topographically arranged within the superior colliculus and the lateral geniculate nucleus (Udin and Fawcett, 1988). Thus, the

NGF Eye Administration Recovers the TrkB and Glutamate/GABA Marker Deficit in the Adult Visual Cortex Following Optic Nerve Crush

“…In vitro and in vivo studies demonstrated that in developing visual system, Nogo plays a role in directing uncrossed axons to the ipsilateral optic tract, and that perturbation of Nogo receptor (NgR1) retina expression might results in alteration of normal axon crossing and non-crossing route at midline chiasma [ 54 , 55 ]. Whether a similar mechanism might occur in adults, and/or following retina deafferentation is still unclear.…”