Flavonoid modulation of ionic currents mediated by GABAA and GABAC receptors

JUAN D. GOUTMAN; MAXIMILIANO D. WAXEMBERG; FRANCISCO DOÑATE-OLIVER; PABLO E. POMATA; DANIEL J. CALVO

EUROPEAN JOURNAL OF PHARMACOLOGY

Año: 2003 vol. 461 p. 79 - 87

0014-2999

The modulation of ionotropic g-aminobutyric acid (GABA) receptors (GABA-gated Cl
channels) by a group of natural and synthetic flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and g-aminobutyric acid (GABA) receptors (GABA-gated Cl
channels) by a group of natural and synthetic flavonoids was studied in electrophysiological experiments. Quercetin, apigenin, morine, chrysin and flavone inhibited ionic currents mediated by a1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA anda1h1g2s GABAA and U1 GABAC receptors expressed in Xenopus laevis oocytes in the micromolar range. a1h1g2s GABAA and U1 GABAC receptors differ largely in their sensitivity to benzodiazepines, but they were similarly modulated by different flavonoids. Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA 1 GABAC receptors differ largely in their sensitivity to benzodiazepines, but they were similarly modulated by different flavonoids. Quercetin produced comparable actions on currents mediated by a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAA a4h2 neuronal nicotinic acetylcholine, serotonin 5-HT3A and glutamate AMPA/kainate receptors. Sedative and anxiolytic flavonoids, like chrysin or apigenin, failed to potentiate but antagonized a1h1g2s GABAAa1h1g2s GABAA receptors. Effects of apigenin and quercetin on a1h1