Abstract
The influence of chlormethiazole, on currents evoked by γ-aminobutyric acid (GABA) and glycine, was investigated under voltage-clamp conditions, in bovine chromaffin cells and murine spinal neurones, respectively. Chlormethiazole (30 and 100 μM) 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 μM)-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.
Original language | English |
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Pages (from-to) | 239-246 |
Number of pages | 8 |
Journal | European Journal of Pharmacology |
Volume | 210 |
Issue number | 3 |
DOIs | |
Publication status | Published - 21 Jan 1992 |
Keywords
- Anaesthetics (general)
- Anticonvulsants
- Chlormethiazole
- GABA receptors
- Glycine receptors
- Patch-clamp
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Pharmacology