K.–F. So

Localization of p75 neurotrophin receptor in the retina of the adult SD rat: an immunocytochemical study at light and electron microscopic levels.

The low‐affinity neurotrophin receptor p75NTR, or p75, is a 75‐kDa cell surface glycoprotein that binds all neurotrophins with similar affinity and is thought to help to ensure the specificity of each neurotrophin. In order to better understand the role of p75 and how it is involved in the neurotrophic effects in the retina, we have examined its cellular localization in the adult rat retina by immunocytochemistry at both light and electron microscopic levels. The similarity between the staining pattern of p75 and that of the distribution of Müller cell processes, as marked by antibodies against S‐100 and vimentin, suggests that p75 may be on the Müller cell processes and not on the retinal ganglion cells (RGCs) as previously reported. The failure to detect p75 immunoreactivity on Fluoro‐Gold retrogradely labeled RGCs in the radially sectioned retinae also indicates that it is not expressed on RGCs. The results from the light microscopic immunohistochemical studies are supported at the ultrastructural level, showing that p75‐immunopositive staining is localized on Müller cell processes and not on RGC bodies. Müller cell processes not only form the inner limiting membrane but also partially wrap around the RGC bodies. Our results lead us to conclude that the previously reported immunopositive staining of p75 on RGCs might belong to the surrounding Müller cell processes. Thus, the pathway of neurotrophic effects on RGCs might be, at least partially, through a glial–neuronal pathway rather than on RGCs directly. GLIA 24:187–197, 1998.

The Potential Role of Nitric Oxide Synthase in Survival and Regeneration of Magnocellular Neurons of Hypothalamo-Neurohypophyseal System

Previous investigations from this laboratory have demonstrated that hypophysectomy induces up-regulation of neuronal nitric oxide synthase (nNOS) in magnocellular neurons of the mammalian hypothalamo-neurohypophyseal system (HNS). Accompanied by this upregulation of nNOS, both neuronal regeneration and degeneration are also observed in this system following hypophysectomy. The specific aim of this study was to determine the potential role of nNOS upregulation in neuronal survival and regeneration after hypophysectomy in the adult Sprague–Dawley (SD) rat by using a competitive nitric oxide synthase blocker, N(G)-nitrol-l-arginine methyl ester (l-NAME). We found that l-NAME treatment effectively blocked the regeneration of magnocellular neurons of the rodent hypothalamus as observed in the lumen of the third cerebral ventricle following hypophysectomy. However, l-NAME had no effect on the survival of magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei after hypophysectomy. These results suggest that the induced increase of nNOS expression enhance the regenerative ability of magnocellular neurons of the HNS following hypophysectomy.