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Glutamine synthetase (GS) activity and spatial and temporal patterns of GS expression in the developing chick retina: Relationship with synaptogenesis in the outer plexiform layer
Author(s) -
Prada Francisco A.,
Quesada Adela,
Dorado Manuel E.,
Chmielewski Carola,
Prada Carmen
Publication year - 1998
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199803)22:3<221::aid-glia2>3.0.co;2-8
Subject(s) - synaptogenesis , biology , glutamine synthetase , retina , inner plexiform layer , outer plexiform layer , neuroscience , microbiology and biotechnology , glutamine , biochemistry , amino acid
The profile of glutamine synthetase (GS) activity in the neural retina of chicken embryos and adults was studied alongside the in vivo spatio‐temporal patterns of generation and morphogenesis of Müller cell and of retinal synaptogenesis. The rise of GS activity during development is not related to Müller cell differentiation but to synaptogenesis in the outer plexiform layer (opl). GS expression was investigated by immunoreaction with GS‐specific antiserum. Three spatial gradients of decreasing labeling were observed between embryonic (E)15 and E18, from central to peripheral retina, dorsal to ventral, and temporal to nasal, which are in spatio‐temporal relationship with synaptogenesis in the opl. GS is localized in Müller cells and apparently also in a population of astrocyte‐like glial cells, located in the ganglion cell layer throughout the retina. Precocious induction by hydrocortisone, in ovo, at E10, does not show the spatial pattern of GS immunoreactivity observed in control retinas at the time of natural induction (E15). We also show that dissociated (non‐cultured) Müller cells of E18–20 retinas, to which only photoreceptors or photoreceptors and neurons remain joined, maintain an immunodetectable level of GS, while those in isolated state lose GS immunoreactivity rapidly. Our results suggest that the induction of GS expression might be mediated by Müller cell‐neuron interactions at the opl and also perhaps at the outer nuclear layer (onl). An analysis of our results and those of previous authors suggests that the level of GS in differentiated Müller cells could be determined by conjoint cell interactions at the onl, opl, and inner plexiform layer. GLIA 22:221–236, 1998. © 1998 Wiley‐Liss, Inc.

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