Injury to retinal ganglion cell axons increases polysialylated neural cell adhesion molecule (PSA-NCAM) in the adult rodent superior colliculus.

Abstract The adult mammalian central nervous system (CNS) exhibits a limited regenerative response to injury. It is well established that polysialylated neural cell adhesion molecule (PSA-NCAM) contributes to nervous system plasticity. In the visual system, PSA-NCAM participates in retinal ganglion cell (RGC) axon growth during development and specifically influences RGC innervation of its principle target tissue, the superior colliculus (SC). The goals of this study were to determine whether PSA-NCAM is expressed in the normal adult mouse SC and to evaluate PSA-NCAM expression following RGC injury. In the normal rostral, but not caudal, SC we find that PSA-NCAM is present in the retinorecipient layers; however, PSA-NCAM and RGC axons do not co-localize. In the deeper collicular layers, PSA-NCAM is observed as several distinct patches that occur at the same depth along the medial–lateral axis throughout the colliculus. RGC axotomy denervates predominantly the contralateral colliculus, where increased PSA-NCAM levels are seen at 7 and 10 days after the injury. Further evaluation of the retinorecipient layers of the partially denervated SC reveals that some intact CTB-traced RGC axons (less than 5%) labeled from the ipsilateral eye do co-localize with PSA-NCAM. This study is the first characterization of PSA-NCAM expression in the normal and partially denervated adult SC and may indicate that PSA-NCAM is involved in attempted visual system remodeling after injury.