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dc.contributor.author김원기-
dc.date.accessioned2018-06-02T08:15:48Z-
dc.date.available2018-06-02T08:15:48Z-
dc.date.issued2007-
dc.identifier.issn0920-1211-
dc.identifier.otherOAK-3901-
dc.identifier.urihttps://dspace.ewha.ac.kr/handle/2015.oak/244661-
dc.description.abstractWe examined whether (-)-nicotine infusion can affect kainic acid (KA)-induced neurotoxicity in rats. Although treatment with a single nicotine infusion (0.5 or 1.0 μg/side, i.c.v.) failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 μg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration. α-Bungarotoxin and mecamylamine blocked the neuroprotective effects of nicotine. These results suggest that repeated nicotine treatment provides α7 nicotinic acetylcholine receptor-mediated neuroprotection against KA toxicity. © 2006 Elsevier B.V. All rights reserved.-
dc.languageEnglish-
dc.titleRepeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor-
dc.typeArticle-
dc.relation.issue3-
dc.relation.volume73-
dc.relation.indexSCI-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage292-
dc.relation.lastpage298-
dc.relation.journaltitleEpilepsy Research-
dc.identifier.doi10.1016/j.eplepsyres.2006.11.004-
dc.identifier.wosidWOS:000245322400010-
dc.identifier.scopusid2-s2.0-33847189602-
dc.author.googleShin E.-J.-
dc.author.googleChae J.S.-
dc.author.googleJung M.-E.-
dc.author.googleBing G.-
dc.author.googleKo K.H.-
dc.author.googleKim W.-K.-
dc.author.googleWie M.B.-
dc.author.googleCheon M.-A.-
dc.author.googleNah S.-Y.-
dc.author.googleKim H.-C.-
dc.contributor.scopusid김원기(34770946200)-
dc.date.modifydate20211210152058-
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자연과학대학 > 화학·나노과학전공 > Journal papers
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