Excitatory amino acid-induced phosphoinositide hydrolysis in Müller glia

✍ Scribed by Dr. Ana María López-Colomé; Arturo Ortega; Mónica Romo-De-Vivar

• Publisher: John Wiley and Sons
• Year: 1993
• Tongue: English
• Weight: 953 KB
• Volume: 9
• Category: Article
• ISSN: 0894-1491
• DOI: 10.1002/glia.440090206

✦ Synopsis

The presence of excitatory amino acid ( E M ) receptors coupled to phosphoinositide metabolism in primary cultures of Muller (glial) cells from the chick retina was established. The order of potency of analogues for stimulating [3Hlinositol phosphate (IP) accumulation was quisqualate (QA) > L-glutamate (L-Glu) = kainate (KA) > N-methyl-D-aspartate (NMDA) > L-aspartate (L-Asp) with EC,, in the range of 1-100 pM. l-Aminocyclopentane-1,3-dicarboxylate (trans-ACPD), u-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), 2-amino-3-phosphonopropionate (AF'3), and 2-amino-4phosphonobutyrate (AP4) showed no effect either on basal concentration or on stimulated accumulation of ["HIIPs. The effect of EAA was potently inhibited by the ionotropic NMDA receptor antagonists 2-amino-5-phosphonopentanoate (AP5), 3-[(RS)-Zcarboxypiperazin-4-yl)l-propyl-1-phosphonate (CPP), and ( + )-5-methyI-lO,ll-dihydro-5H-dibenzo[a,d]cyclohepten-5-1O-imine (MK-801); L-Glu antagonists at non-NMDA receptors, the quinoxalines NBQX and DNQX, inhibited weakly the response to L-Glu, KA, and NMDA, and more potently that to &A. The translocation of protein kinase C was also stimulated by EAA with the same pharmacological profile, and was partially inhibited by kynurenate (KYN). L-Glu and KA induced 45Ca2+ influx, which was decreased by IPs accumulation was decreased by verapamil but not by nifedipine, and slightly diminished by dantrolene. Results demonstrate that EAA-induced phosphoinositide hydrolysis in Muller cells shows pharmacological differences with that in astrocytes and neuronal cells and could be triggered by a different mechanism.