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Modulation of GABAA and glycine receptors by chlormethiazole.
Hales, T G; Lambert, J J.
Afiliación
  • Hales TG; Department of Anesthesiology, Medical Center, UCLA 90024.
Eur J Pharmacol ; 210(3): 239-46, 1992 Jan 21.
Article en En | MEDLINE | ID: mdl-1319334
The influence of chlormethiazole, on currents evoked by gamma-aminobutyric acid (GABA) and glycine, was investigated under voltage-clamp conditions, in bovine chromaffin cells and murine spinal neurones, respectively. Chlormethiazole (30 and 100 microM) dose dependently potentiated currents activated by either inhibitory neurotransmitter. The potentiation of the GABA-evoked response occurred without altering the reversal potential and was not influenced by the benzodiazepine receptor antagonist Ro 15-1788 (300 nM). GABA-gated channels, recorded from outside-out membrane patches, showed increased probability of being in the conducting state in the presence of chlormethiazole. High concentrations of chlormethiazole (3 mM) activated bicuculline (1 microM)-sensitive whole-cell currents with a reversal potential similar to the chloride equilibrium potential. Chlormethiazole potentiates GABA- and glycine-activated currents and at higher doses, directly activates the GABAA receptor.
Asunto(s)
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Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Clormetiazol / Receptores de GABA-A Límite: Animals Idioma: En Revista: Eur J Pharmacol Año: 1992 Tipo del documento: Article
Buscar en Google
Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Clormetiazol / Receptores de GABA-A Límite: Animals Idioma: En Revista: Eur J Pharmacol Año: 1992 Tipo del documento: Article