CELLULAR-LOCALIZATION OF GLUR1, GLUR2 3 AND GLUR4 GLUTAMATE-RECEPTOR SUBUNITS IN NEURONS OF THE RAT NEOSTRIATUM/

Citation
Khh. Kwok et al., CELLULAR-LOCALIZATION OF GLUR1, GLUR2 3 AND GLUR4 GLUTAMATE-RECEPTOR SUBUNITS IN NEURONS OF THE RAT NEOSTRIATUM/, Brain research, 778(1), 1997, pp. 43-55
Citations number
54
Journal title
ISSN journal
00068993
Volume
778
Issue
1
Year of publication
1997
Pages
43 - 55
Database
ISI
SICI code
0006-8993(1997)778:1<43:COGG3A>2.0.ZU;2-4
Abstract
Glutamate excitocytotoxicity is implied in the cause of neuronal degen eration in the neostriatum, in which the toxicity may be mediated by d ifferent families of glutamate receptors. The precise cellular localiz ation of ha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA)-typ e glutamate receptor subunits (GluR1-4), one of the major family that involves in the mechanisms of glutamate excitocytotoxicity, in differe nt populations of striatal neurons is therefore of special interest. I mmunoreactivity for GluR2/3 subunits was detected in the medium-sized spiny neurons. By double labelling experiments, immunoreactivity for G luR1 and GluR4 was detected only in aspiny striatal neurons that displ ay parvalbumin immunoreactivity, but not in the other neuron populatio ns that display choline acetyltransferase or muscarinic m2 receptor im munoreactivity, nor neurons that display nitric oxide synthase immunor eactivity or nicotinamide adenine dinucleotide phosphate-diaphorase ac tivity. These results indicate that GluR1 and GluR4 immunoreactivity i s displayed only in the GABAergic interneurons in the neostriatum. In addition, almost all of the GluR1-immunoreactive neurons were found to display GluR4 immunoreactivity. This finding indicates for the first time that the striatal GABAergic interneurons co-express GluR1 and Glu R4 subunits. The results of the present study indicate that there is a differential localization of AMPA-type glutamate receptor subunits in different populations of striatal neurons and they may have a differe nt susceptibility to glutamate excitocytotoxicity. (C) 1997 Elsevier S cience B.V.