Abstract. Peripheral nerve injury results in short-term and long-term changes in both neurons and glia. In the present study, immunohistological and immunoblot analyses were used to examine the expression of the neural cell adhesion molecule (N-CAM) and the neuron-glia cell adhesion molecule (Ng

We have compared the expression of the neural cell adhesion molecule (N-CAM) and the neuron-glial cell adhesion molecule (Ng-CAM) during histogenesis of the chick nervous system. Data from immunohistochemistry and photometry were combined to construct maps of the overall distribution and dynamics of CAM appearance and disappearance. Each CAM appeared in a characteristic spatial and temporal pattern in various areas during cell movement, fiber outgrowth, tract formation, and myelination. N-CAM was more uniformly distributed than Ng-CAM and was present on all neural cell bodies and processes of the CNS and PNS. In the adult, the staining pattern of N-CAM remained similar to that in the embryo, although the staining intensity was diminished. During embryonic development, Ng-CAM was expressed on extending neurites and migrating neurons. The appearance Ng-CAM in the CNS was correlated particularly with times of cell migration in spinal cord and cerebellum, and in regions undergoing neurite extension, such as the developing white matter of the spinal cord, the optic nerve, and the medial longitudinal fasciculus. Cell bodies not undergoing migration were negative for Ng-CAM. In the adult CNS, Ng-CAM was markedly decreased in myelinated fiber tracts like the white matter of the spinal cord but persisted in unmyelinated regions such as the olfactory bulb. In contrast, in the PNS (for example, the dorsal root ganglion and sciatic nerve), Ng-CAM appeared early on both cell bodies and neurites, and it continued to be present on both in the adult, even in the presence of myelin. Maps comparing the relative distribution of Ng-CAM and N-CAM showed dynamic reversals as the nervous system developed and, as a result, the pattern of CAM expression was markedly different in embryos and adults. This difference appears to reflect changes in the roles of selective adhesion and of the two neuronal CAMs at different times of development.

Abstract. Immunocytochemical methods were used toshow that Ng-CAM (the neuron-glia cell adhesion molecule), N-CAM (the neural cell adhesion molecule), and the extracellular matrix protein cytotactin are highly concentrated at nodes of Ranvier of the adult chicken and mouse. In contrast, unmyelinated axonal fibers were uniformly stained by specific antibodies to both CAMs but not by antibodies to cytotactin. Ultrastructural immunogold techniques indicated that both N-CAM and Ng-CAM were enriched in the nodal axoplasm and axolemma of myelinated fibers as well as within the nodal regions of the myelinating Schwann cell. At embryonic day 14, before myelination had occurred, small-caliber fibers of chick embryos showed periodic coincident accumulations of the two CAMs but not of cytotactin, with faint labeling in the axonal regions between accumulations. Cytotactin was found on Schwann cells and in connective tissue. By embryonic day 18, nodal accumulations of CAMs were first observed in a few medium-and large-caliber fibers. Immunoblot analyses indicated that embryonic to adult conversion of N-CAM and a progressive decrease in the amount of Ng-CAM and N-CAM occurred while nodes were forming. Sciatic nerves of mouse mutants with defects in cell interactions showed abnormalities in the distribution patterns and amount of Ng-CAM, N-CAM, and cytotactin that were consistent with the known morphological nodal disorders. In trembler (+/Tr), intense staining for both CAMs appeared all along the fibers and the amounts of N-CAM in the sciatic nerve were found to be increased. In mice with motor endplate disease (med/med), Ng-CAM and N-CAM, but not cytotactin, were localized in the widened nodes. Both trembler and med/med Schwann cells stained intensely for cytotactin, in contrast to normal Schwann cells which stained only slightly. All of these findings are consistent with the hypothesis that surface modulation of neuronal CAMs mediated by signals shared between neurons and glia may be necessary for establishing and maintaining the nodes of Ranvier.

This study evaluated the ability of Schwann cell transplants to enhance the recovery of function in injured nerves and compared the results to those produced by sural nerve grafts. Schwann cells were isolated from sciatic nerves, prelabeled with gold fluorescent dye admixed with collagen gel, and placed in resorbable collagen tubes. Twenty-four adult rats underwent severing of the bilateral sciatic nerves, with a 10-mm gap between the nerve stumps. The rats were then divided into two groups. A collagen tube with implanted Schwann cells was implanted in one leg of the Group I rats, and the contralateral leg served as a control and was repaired with a collagen tube filled with collagen gel only. The Group II animals received conduits packed with labeled Schwann cells in one leg to bridge the 10-mm gap; the contralateral leg was repaired with an autogenous sural nerve graft. Recovery of function was assessed physiologically and morphologically. Nerve conduction velocity and nerve action potential amplitude measurements showed that the Schwann cell implants induced return of function comparable to that of the sural nerve grafts. Morphological assessments of myelination suggested a tendency toward greater numbers of myelinated axons in Schwann cell implants than in sural nerve grafts. Anatomical analyses of gold fluorescent dye showed both high viability of prelabeled Schwann cells at 120 days after transplantation and migration as far as 30 mm away from the implant site.

Abstract. Cytotactin is an extracellular glycoprotein found in a highly specialized distribution during embryonic development. In the brain, it is synthesized by glia, not neurons. It is involved in neuron-glia adhesion in vitro and affects neuronal migration in the developing cerebellum. In an attempt to extend these observations to the peripheral nervous system, we have examined the distribution and localization of cytotactin in different parts of the normal and regenerating neuromuscular system. In the normal neuromuscular sys-