title: Glutamate increases the [Ca2+]i but stimulates Ca(2+)-independent release of [3H]GABA in cultured chick retina cells.
abstract: The effect of glutamate on [Ca2+]i and on [3H] gamma-aminobutyric acid (GABA) release was studied on cultured chick embryonic retina cells. It was observed that glutamate (100 microM) increases the [Ca2+]i by Ca2+ influx through Ca2+ channels sensitive to nitrendipine, but not to omega-conotoxin GVIA (omega-Cg Tx) (50%), and by other channels insensitive to either Ca2+ channel blocker. Mobilization of Ca2+ by glutamate required the presence of external Na+, suggesting that Na+ mobilization through the ionotropic glutamate receptors is necessary for the Ca2+ channels to open. The increase in [Ca2+]i was not related to the release of [3H]GABA induced by glutamate, suggesting that the pathway for the entry of Ca2+ triggered by glutamate does not lead to exocytosis. In fact, the glutamate-induced release of [3H]GABA was significantly depressed by Ca(2+)o, but it was dependent on Na(+)o, just as was observed for the [3H]GABA release induced by veratridine (50 microM). The veratridine-induced release could be fully inhibited by TTX, but this toxin had no effect on the glutamate-induced [3H]GABA release. Both veratridine- and glutamate-induced [3H]GABA release were inhibited by 1-(2-(((diphenylmethylene)amino)oxy)ethyl)-1,2,5,6-tetrahydro-3-py ridine- carboxylic acid (NNC-711), a blocker of the GABA carrier. Blockade of the NMDA and non-NMDA glutamate receptors with MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), respectively, almost completely blocked the release of [3H]GABA evoked by glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Zoology, University of Coimbra, Portugal.
authors.forename: C B
authors.initials: CB
authors.lastname: Duarte
authors.forename: I L
authors.initials: IL
authors.lastname: Ferreira
authors.forename: P F
authors.initials: PF
authors.lastname: Santos
authors.forename: C R
authors.initials: CR
authors.lastname: Oliveira
authors.forename: A P
authors.initials: AP
authors.lastname: Carvalho
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002478:Cells, Cultured; D002642:Chick Embryo; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D009539:Nicotinic Acids / Q000494:pharmacology; D009557:Nipecotic Acids; D009568:Nitrendipine / Q000494:pharmacology; D010091:Oximes / Q000494:pharmacology; D010455:Peptides / Q000494:pharmacology; D012160:Retina / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D014701:Veratridine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*; D020866:omega-Conotoxin GVIA
chemical_list: D002121:Calcium Channel Blockers; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D009539:Nicotinic Acids; D009557:Nipecotic Acids; D010091:Oximes; D010455:Peptides; C078793:NNC 711; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D014701:Veratridine; D020866:omega-Conotoxin GVIA; D009568:Nitrendipine; D002118:Calcium