Altered long-term potentiation in the hippocampus of apolipoprotein E-deficient mice

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dc.contributor.authorVeinbergs, Iko
dc.contributor.authorJung, MWko
dc.contributor.authorYoung, SJko
dc.contributor.authorVan Uden, Eko
dc.contributor.authorGroves, PMko
dc.contributor.authorMasliah, Eko
dc.date.accessioned2013-03-03T08:58:13Z-
dc.date.available2013-03-03T08:58:13Z-
dc.date.created2013-02-20-
dc.date.created2013-02-20-
dc.date.issued1998-06-
dc.identifier.citationNEUROSCIENCE LETTERS, v.249, no.2-3, pp.71 - 74-
dc.identifier.issn0304-3940-
dc.identifier.urihttp://hdl.handle.net/10203/78087-
dc.description.abstractRecent studies suggest that apolipoprotein E (apoE) plays a neurotrophic role in the central nervous system and that an aberrant function of this molecule might result in neurodegeneration. Supporting this notion, apoE-deficient mice show neurodegenerative and cognitive alterations. To characterize physiological changes associated with synaptic damage and cognitive impairment in apoE-deficient mice, we investigated synaptic plasticity in the hippocampus of urethane anesthetized mice. Electrical stimulation was delivered to the perforant pathway and the resulting evoked field excitatory postsynaptic potential (EPSP) and population spike were recorded in the hilus. Long-term potentiation, as measured in the population spike, was reduced by 50% in apoE-deficient mice when compared to wild-type controls. In contrast, there were no significant differences in the evoked field EPSP between wild-type and apoE-deficient mice following high-frequency stimulation. These results support the notion that cognitive impairment and synaptic loss in the hippocampus of apoE-deficient mice might be associated with impaired long-term potentiation. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.-
dc.languageEnglish-
dc.publisherELSEVIER SCI IRELAND LTD-
dc.subjectALZHEIMERS-DISEASE-
dc.titleAltered long-term potentiation in the hippocampus of apolipoprotein E-deficient mice-
dc.typeArticle-
dc.identifier.wosid000074745500001-
dc.identifier.scopusid2-s2.0-0032547137-
dc.type.rimsART-
dc.citation.volume249-
dc.citation.issue2-3-
dc.citation.beginningpage71-
dc.citation.endingpage74-
dc.citation.publicationnameNEUROSCIENCE LETTERS-
dc.identifier.doi10.1016/S0304-3940(98)00399-1-
dc.contributor.localauthorJung, MW-
dc.contributor.nonIdAuthorVeinbergs, I-
dc.contributor.nonIdAuthorYoung, SJ-
dc.contributor.nonIdAuthorVan Uden, E-
dc.contributor.nonIdAuthorGroves, PM-
dc.contributor.nonIdAuthorMasliah, E-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorneurodegeneration-
dc.subject.keywordAuthordendritic vacuolization-
dc.subject.keywordAuthorapolipoprotein E-
dc.subject.keywordAuthorsynapse-
dc.subject.keywordAuthorknockout-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
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