LOCALIZATION OF P75 NEUROTROPHIN RECEPTOR IN THE RETINA OF THE ADULT SD RAT - AN IMMUNOCYTOCHEMICAL STUDY AT LIGHT AND ELECTRON-MICROSCOPICLEVELS

Authors
Citation
B. Hu et al., LOCALIZATION OF P75 NEUROTROPHIN RECEPTOR IN THE RETINA OF THE ADULT SD RAT - AN IMMUNOCYTOCHEMICAL STUDY AT LIGHT AND ELECTRON-MICROSCOPICLEVELS, Glia, 24(2), 1998, pp. 187-197
Citations number
77
Categorie Soggetti
Neurosciences
Journal title
GliaACNP
ISSN journal
08941491
Volume
24
Issue
2
Year of publication
1998
Pages
187 - 197
Database
ISI
SICI code
0894-1491(1998)24:2<187:LOPNRI>2.0.ZU;2-J
Abstract
The low-affinity neurotrophin receptor p75(NTR), or p75, is a 75-kDa c ell surface glycoprotein that binds all neurotrophins with similar aff inity and is thought to help to ensure the specificity of each neurotr ophin. In order to better understand the role of p75 and how it is inv olved in the neurotrophic effects in the retina, we have examined its cellular localization in the adult rat retina by immunocytochemistry a t both light and electron microscopic levels. The similarity between t he staining pattern of p75 and that of the distribution of Muller cell processes, as marked by antibodies against S-100 and vimentin, sugges ts that p75 may be on the Muller cell processes and not on the retinal ganglion cells (RGCs) as previously reported. The failure to detect p 75 immunoreactivity on Fluoro-Gold retrogradely labeled RGCs in the ra dially sectioned retinae also indicates that it is not expressed on RG Cs. The results from the light microscopic immunohistochemical studies are supported at the ultrastructural level, showing that p75-immunopo sitive staining is localized on Muller cell processes and not on RGC b odies. Muller 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 Muller cell processes. Thus, t he pathway of neurotrophic effects on RGCs might be, at least partiall y, through a glial-neuronal pathway rather than on RGCs directly. (C) 1998 Wiley-Liss, Inc.