Abstract |
This study examined the nature of the interactions of etifoxine, an anxiolytic and anticonvulsant compound, with the GABA(A) receptor/chloride channel complex. In membrane preparations of Sprague-Dawley rat cerebral cortex, etifoxine competitively inhibited the binding of [35S]t-butylbicyclophosphoro-thionate (TBPS), a specific ligand of the GABA(A) receptor chloride channel site. In vivo studies demonstrated an anticonvulsant effect of etifoxine (50 and 75 mg/kg, i.p.) against the clonic convulsions induced by TBPS in CD1 mice. Flumazenil (10 and 40 mg/kg, i.p.), an antagonist of benzodiazepine sites at GABA(A) receptors, had no effect on the action of etifoxine. These findings suggest that etifoxine exerts its effect by interacting with the Cl- channel of GABA(A) receptors and probably by facilitating GABAergic inhibition.
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Authors | M Verleye, R Schlichter, J M Gillardin |
Journal | Neuroreport
(Neuroreport)
Vol. 10
Issue 15
Pg. 3207-10
(Oct 19 1999)
ISSN: 0959-4965 [Print] England |
PMID | 10574561
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Anticonvulsants
- Bridged Bicyclo Compounds, Heterocyclic
- Chloride Channels
- Convulsants
- GABA Modulators
- Oxazines
- Receptors, GABA-A
- Flumazenil
- tert-butylbicyclophosphorothionate
- etifoxine
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Topics |
- Animals
- Anticonvulsants
(pharmacology)
- Binding, Competitive
(drug effects, physiology)
- Bridged Bicyclo Compounds, Heterocyclic
(pharmacology)
- Cell Membrane
(drug effects, physiology)
- Cerebral Cortex
(metabolism, physiology)
- Chloride Channels
(drug effects, physiology)
- Convulsants
(pharmacology)
- Flumazenil
(pharmacology)
- GABA Modulators
(pharmacology)
- Kinetics
- Male
- Mice
- Oxazines
(pharmacology)
- Radioligand Assay
- Rats
- Rats, Sprague-Dawley
- Receptors, GABA-A
(drug effects, physiology)
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