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GABAB, not GABAA receptors play a role in cortical postictal refractoriness
P. Mareš, H. Kubová,
Language English Country England, Great Britain
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
- MeSH
- GABA-A Receptor Antagonists pharmacology MeSH
- GABA-B Receptor Antagonists pharmacology MeSH
- Azepines pharmacology MeSH
- Bicuculline pharmacology MeSH
- Electric Stimulation MeSH
- Epilepsy drug therapy physiopathology MeSH
- Electrodes, Implanted MeSH
- Cerebral Cortex drug effects physiopathology MeSH
- Organophosphorus Compounds pharmacology MeSH
- Pentylenetetrazole pharmacology MeSH
- Picrotoxin pharmacology MeSH
- Rats, Wistar MeSH
- Receptors, GABA-A metabolism MeSH
- Receptors, GABA-B metabolism MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
Postictal refractoriness may be taken as an expression of lasting activity of inhibitory systems arresting seizures. We tested drugs interfering with GABAergic inhibitory system in pairs of cortical epileptic afterdischarges induced with 1-min interval in rats. Under control conditions the second stimulation failed to elicit an afterdischarge. This postictal refractoriness was not affected by antagonists of GABAA receptors acting at three binding sites (bicuculline, picrotoxin, benzodiazepine inverse agonist Ro 19-4603) as well as by a less specific antagonist pentetrazol. In contrast, antagonist of GABAB receptors CGP35348 partially blocked the refractoriness. Cooperation of different inhibitory systems is probably necessary to abolish postictal refractoriness in neocortex. This article is part of the Special Issue entitled 'GABAergic Signaling in Health and Disease'.
References provided by Crossref.org
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- $a Postictal refractoriness may be taken as an expression of lasting activity of inhibitory systems arresting seizures. We tested drugs interfering with GABAergic inhibitory system in pairs of cortical epileptic afterdischarges induced with 1-min interval in rats. Under control conditions the second stimulation failed to elicit an afterdischarge. This postictal refractoriness was not affected by antagonists of GABAA receptors acting at three binding sites (bicuculline, picrotoxin, benzodiazepine inverse agonist Ro 19-4603) as well as by a less specific antagonist pentetrazol. In contrast, antagonist of GABAB receptors CGP35348 partially blocked the refractoriness. Cooperation of different inhibitory systems is probably necessary to abolish postictal refractoriness in neocortex. This article is part of the Special Issue entitled 'GABAergic Signaling in Health and Disease'.
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