Abstract
Effective prophylaxis for post-traumatic epilepsy currently does not exist, and clinical trials using anticonvulsant drugs have yielded no long-term antiepileptogenic effects. We report that a single, rapid post-traumatic application of the proconvulsant cannabinoid type-1 (CB1) receptor antagonist SR141716A (Rimonabant-Acomplia) abolishes the long-term increase in seizure susceptibility caused by head injury in rats. These results indicate that, paradoxically, a seizure-enhancing drug may disrupt the epileptogenic process if applied within a short therapeutic time window.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Anticonvulsants / therapeutic use
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Craniocerebral Trauma / complications
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Craniocerebral Trauma / drug therapy*
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Disease Models, Animal
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Electroencephalography / methods
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Epilepsy, Post-Traumatic / etiology
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Epilepsy, Post-Traumatic / prevention & control*
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Pentobarbital / therapeutic use
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Piperidines / therapeutic use*
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Pyrazoles / therapeutic use*
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Rats
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Rats, Wistar
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Receptor, Cannabinoid, CB1 / antagonists & inhibitors*
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Rimonabant
Substances
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Anticonvulsants
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Piperidines
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Pyrazoles
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Receptor, Cannabinoid, CB1
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Pentobarbital
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Rimonabant