Abstract
Lethargic (lh/lh) mice, which function as an animal model of absence seizures, have spontaneous seizures that have behavioral and electrographic features and anticonvulsant sensitivity similar to those of human absence seizures. Antagonists of the gamma-aminobutyric acidB (GABAB) receptor suppressed these seizures in lethargic mice, whereas agonists of GABAB receptors exacerbated them. Furthermore, GABAB receptor binding and synaptically evoked GABAB receptor-mediated inhibition of N-methyl-D-aspartate responses were selectively increased in lh/lh mice. Therefore, enhanced GABAB receptor-mediated synaptic responses may underlie absence seizures in lh/lh mice, and GABAB receptor antagonists hold promise as anticonvulsants for absence seizures.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Anticonvulsants / pharmacology
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Baclofen / analogs & derivatives
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Baclofen / pharmacology
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Disease Models, Animal
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Dose-Response Relationship, Drug
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Electroencephalography
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Electrophysiology
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Epilepsy, Absence / drug therapy
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Epilepsy, Absence / physiopathology*
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Hippocampus / drug effects
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Hippocampus / physiology
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In Vitro Techniques
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Mice
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Mice, Inbred Strains
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Organophosphorus Compounds / pharmacology
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Picrotoxin / pharmacology
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Quinoxalines / pharmacology
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Receptors, GABA-A / physiology*
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Receptors, N-Methyl-D-Aspartate / metabolism
Substances
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Anticonvulsants
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Organophosphorus Compounds
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Quinoxalines
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Receptors, GABA-A
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Receptors, N-Methyl-D-Aspartate
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Picrotoxin
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FG 9041
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CGP 35348
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Baclofen
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2-hydroxysaclofen