INVESTIGADORES
GOUTMAN Juan Diego
artículos
Título:
Flavonoid modulation of ionic currents mediated by GABAA and GABAC receptors
Autor/es:
JUAN D. GOUTMAN; MAXIMILIANO D. WAXEMBERG; FRANCISCO DOÑATE-OLIVER; PABLO E. POMATA; DANIEL J. CALVO
Revista:
EUROPEAN JOURNAL OF PHARMACOLOGY
Referencias:
Año: 2003 vol. 461 p. 79 - 87
ISSN:
0014-2999
Resumen:
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