Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:1281937rdf:typepubmed:Citationlld:pubmed
pubmed-article:1281937lifeskim:mentionsumls-concept:C0037473lld:lifeskim
pubmed-article:1281937lifeskim:mentionsumls-concept:C0597329lld:lifeskim
pubmed-article:1281937lifeskim:mentionsumls-concept:C0439799lld:lifeskim
pubmed-article:1281937lifeskim:mentionsumls-concept:C1521840lld:lifeskim
pubmed-article:1281937pubmed:dateCreated1993-1-25lld:pubmed
pubmed-article:1281937pubmed:abstractTextThe symptoms of poisoning by the pyrethroid and cyclodiene insecticides are characterized by hyperexcitation and convulsions followed by paralysis. The main target site of the pyrethroids has been identified to be the sodium channels which are kept open for unusually long periods of time, causing a prolonged sodium current to flow which, in turn, leads to hyperexcitation of the nervous system. We have now found large differential sensitivity to the pyrethroids in two types of sodium channels. The dorsal root ganglion neurons of the rat were endowed with two types of sodium channels, one sensitive to the blocking action of tetrodotoxin (TTX) and the other insensitive to TTX. The type I pyrethroid allethrin and the type II pyrethroid deltamethrin were both effective in prolonging the sodium current in the TXX-resistant sodium channel but had only a small effect on the TTX-sensitive sodium channel. These two types of sodium channels also exhibited marked differences in their physiological properties, including the time course of current, the activation voltage, and the steady-state inactivation. In contrast to the pyrethroids, lindane and the cyclodienes endrin, isobenzan, dieldrin and heptachlor-epoxide suppressed the GABA-induced chloride current. The initial transient component of the chloride current was blocked more than the late sustained component. The suppression of the GABA-mediated synaptic inhibition would cause hyperexcitation of the nervous system. The results are compatible with the convulsant action of these insecticides.lld:pubmed
pubmed-article:1281937pubmed:granthttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:languageenglld:pubmed
pubmed-article:1281937pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:citationSubsetIMlld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:1281937pubmed:statusMEDLINElld:pubmed
pubmed-article:1281937pubmed:monthDeclld:pubmed
pubmed-article:1281937pubmed:issn0378-4274lld:pubmed
pubmed-article:1281937pubmed:authorpubmed-author:NarahashiTTlld:pubmed
pubmed-article:1281937pubmed:authorpubmed-author:RoyM LMLlld:pubmed
pubmed-article:1281937pubmed:authorpubmed-author:GinsburgK SKSlld:pubmed
pubmed-article:1281937pubmed:authorpubmed-author:FreyJ MJMlld:pubmed
pubmed-article:1281937pubmed:issnTypePrintlld:pubmed
pubmed-article:1281937pubmed:volume64-65 Spec Nolld:pubmed
pubmed-article:1281937pubmed:ownerNLMlld:pubmed
pubmed-article:1281937pubmed:authorsCompleteYlld:pubmed
pubmed-article:1281937pubmed:pagination429-36lld:pubmed
pubmed-article:1281937pubmed:dateRevised2007-11-14lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:meshHeadingpubmed-meshheading:1281937-...lld:pubmed
pubmed-article:1281937pubmed:year1992lld:pubmed
pubmed-article:1281937pubmed:articleTitleSodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.lld:pubmed
pubmed-article:1281937pubmed:affiliationDepartment of Pharmacology, Northwestern University Medical School, Chicago, IL 60611.lld:pubmed
pubmed-article:1281937pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1281937pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
pubmed-article:1281937pubmed:publicationTypeReviewlld:pubmed