EXPRESSION OF HIGH-AFFINITY NEURONAL AND GLIAL GLUTAMATE TRANSPORTERSIN THE RAT OPTIC-NERVE

Authors
Citation
I. Choi et Sy. Chiu, EXPRESSION OF HIGH-AFFINITY NEURONAL AND GLIAL GLUTAMATE TRANSPORTERSIN THE RAT OPTIC-NERVE, Glia, 20(3), 1997, pp. 184-192
Citations number
39
Categorie Soggetti
Neurosciences
Journal title
GliaACNP
ISSN journal
08941491
Volume
20
Issue
3
Year of publication
1997
Pages
184 - 192
Database
ISI
SICI code
0894-1491(1997)20:3<184:EOHNAG>2.0.ZU;2-T
Abstract
Recent studies have revealed that a dynamic axon-glial signaling occur s in the rat optic nerve, which is devoid of synapses. This interactio n is postulated to be mediated by non-vesicular release of glutamate v ia a reversal of high-affinity glutamate transporters. Here we examine d the expression of glial glutamate transporters (GLAST and GLT-1) and a neuronal transporter (EAAC1) in the rat optic nerve. RT-PCR analysi s revealed the presence of mRNAs for GLT-1 and GLAST, but not EAAC1. R Nase protection assays showed that of the two glial transporters, mRNA for GLAST was expressed at much higher level than was GLT-1. A simila r expression pattern was found in primary astrocyte culture cells. GLA ST mRNA level in the optic nerve was comparable to that in the cerebel lum. Developmentally, GLAST mRNA level was highest at P2 and dropped s lightly by adulthood. Nerve transection resulted in little or no chang e in mRNA levels for GLAST and GLT-1 assayed at 4 to 14 days post-tran section, but GLAST mRNA level was decreased at 64 days. Western blot a nalysis revealed that the rat optic nerve showed immunoreactivity to a ntibodies against GLT-1, GLAST, and EAAC1. In conclusion, we suggest t hat glial and neuronal transporters are present in the rat optic nerve , where dynamic axon-glial interaction has been known to occur. In par ticular, the unusually high level of expression of GLAST in the optic nerve suggests a possible role for this glial transporter in protectin g optic nerves from neurotoxicity during postnatal. development. (C) 1 997 Wiley-Liss, Inc.