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Antiepileptic Drug Mechanisms of Action
dc.contributor.authorMacdonald, Robert L.en_US
dc.contributor.authorKelly, Kevin M.en_US
dc.date.accessioned2010-04-01T15:47:53Z
dc.date.available2010-04-01T15:47:53Z
dc.date.issued1993-11en_US
dc.identifier.citationMacdonald, Robert L.; Kelly, Kevin M. (1993). "Antiepileptic Drug Mechanisms of Action." Epilepsia 34(): S1-S8. <http://hdl.handle.net/2027.42/66291>en_US
dc.identifier.issn0013-9580en_US
dc.identifier.issn1528-1167en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/66291
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7687957&dopt=citationen_US
dc.description.abstractClinically used antiepileptic drugs (AEDs) decrease membrane excitability by interacting with ion channels or neurotransmitter receptors. Currently available AEDs appear to act on sodium channels, GABA A receptors, or calcium channels. Phenytoin, carbamazepine, and possibly valproate (VPA) decrease high-frequency repetitive firing of action potentials by enhancing sodium channel inactivation. Benzodiazepines and barbiturates enhance GABA A receptor-mediated inhibition. Ethosuximide and possibly VPA reduce a low-threshold calcium current. The mechanisms of action of AEDs currently under development are less clear. Lamotrigine may decrease sustained high-frequency repetitive firing. The mechanisms of action of felbamate are unknown. Gabapentin (GBP) appears to bind to a specific binding site in the central nervous system with a restricted regional distribution, but the identity of the binding site and the mechanism of action of GBP remain uncertain.en_US
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dc.format.extent3110 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Publishing Ltden_US
dc.rights1993 International League Against Epilepsyen_US
dc.subject.otherAnticonvulsantsen_US
dc.subject.otherNeuropharmacologyen_US
dc.subject.otherNeurotransmittersen_US
dc.subject.otherGABAen_US
dc.subject.otherPhenytoinen_US
dc.subject.otherCarbamazepineen_US
dc.subject.otherEthosuximideen_US
dc.subject.otherTri-methadioneen_US
dc.subject.otherBenzodiazepinesen_US
dc.subject.otherBarbituratesen_US
dc.subject.otherValproateen_US
dc.subject.otherFelbamateen_US
dc.subject.otherGabapentinen_US
dc.subject.otherLamotrigineen_US
dc.subject.otherNeural Inhibitionen_US
dc.subject.otherSodiumen_US
dc.subject.otherCalciumen_US
dc.titleAntiepileptic Drug Mechanisms of Actionen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelMedicine (General)en_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum*Departments of Neurology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A.en_US
dc.contributor.affiliationum†Physiology, University of Michigan Medical Center, Ann Arbor, Michigan, U.S.A.en_US
dc.identifier.pmid7687957en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/66291/1/j.1528-1157.1993.tb05918.x.pdf
dc.identifier.doi10.1111/j.1528-1157.1993.tb05918.xen_US
dc.identifier.sourceEpilepsiaen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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