TRANSIENT SOMATOSTATIN-IMMUNOREACTIVE GANGLION-CELLS IN THE DEVELOPING RAT RETINA

Citation
G. Fontanesi et al., TRANSIENT SOMATOSTATIN-IMMUNOREACTIVE GANGLION-CELLS IN THE DEVELOPING RAT RETINA, Developmental brain research, 103(2), 1997, pp. 119-125
Citations number
42
Categorie Soggetti
Neurosciences
ISSN journal
01653806
Volume
103
Issue
2
Year of publication
1997
Pages
119 - 125
Database
ISI
SICI code
0165-3806(1997)103:2<119:TSGITD>2.0.ZU;2-F
Abstract
The peptide somatostatin (SRIF) is likely to play important roles in n euronal differentiation and maturation. In the mammalian retina, it is reported to be expressed by populations of amacrine and/or displaced amacrine cells and, in some species, by some ganglion cells. Previous studies have shown that in the rat retina the maturation of somatostat inergic systems encompasses late prenatal and early postnatal periods, suggesting a role of SRIF in maturative events of the retina. SRIF-ex pressing ganglion cells have not been reported in the rat retina at an y developmental age. In the present study, we re-evaluated the postnat al development of SRIF-containing neurons of the rat retina focusing o n the analysis of SRIF-containing cells in the ganglion cell layer (GC L), to test the possibility that SRIF is expressed by some ganglion ce lls during development. To this aim we combined immunocytochemical sta ining of SRIF-positive neurons with retrograde tracing of ganglion cel l bodies through Fluoro-Gold injections into the superior colliculus. Double-labelling experiments revealed the presence of SRIF-containing ganglion cells at postnatal day (PND) 10. They accounted for 14% of th e total SRIF-containing cells in the GCL. Such double-labelled cells w ere not observed either before (PND 7) or after (PND 15 and PND 45) th is period. This transient expression of SRIF in retinal ganglion cells suggests that SRIF may be a factor regulating the maturation of retin ocollicular projections in a restricted period of postnatal developmen t. (C) 1997 Elsevier Science B.V.