Synaptotagmin and synaptic transmission alterations in apolipoprotein E-deficient mice

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dc.contributor.authorVeinbergs, Iko
dc.contributor.authorMante, Mko
dc.contributor.authorJung, MWko
dc.contributor.authorVan Uden, Eko
dc.contributor.authorMasliah, Eko
dc.date.accessioned2013-03-03T09:16:03Z-
dc.date.available2013-03-03T09:16:03Z-
dc.date.created2013-02-20-
dc.date.created2013-02-20-
dc.date.issued1999-04-
dc.identifier.citationPROGRESS IN NEURO-PSYCHOPHARMACOLOGY BIOLOGICAL PSYCHIATRY, v.23, no.3, pp.519 - 531-
dc.identifier.issn0278-5846-
dc.identifier.urihttp://hdl.handle.net/10203/78155-
dc.description.abstract1. Aged apoE-deficient mice and age-matched controls were tested for cognitive alterations in the Morris water maze. 2. Water maze results were correlated with in vivo electrophysiology and expression of the synaptic protein synaptotagmin (p65). 3. Compared to age-matched controls, apolipoprotein E-deficient mice displayed significant performance impairment accompanied by in vivo electrophysiological alterations in the dentate gyrus. 4. Apolipoprotein B-deficient mice also showed a significant increase in the synaptic protein, synaptotagmin, a synaptic calcium sensor involved in neurotransmitter release. 5. Cognitive impairments in these animals may be associated with decreased synaptic excitability in hippocampal neurons and the regulatory role of apolipoprotein E in synaptic function might be mediated by modulation of the expression of calcium sensor proteins.-
dc.languageEnglish-
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD-
dc.subjectALZHEIMERS-DISEASE-
dc.subjectCHOLINERGIC IMPAIRMENTS-
dc.subjectVESICLE PROTEIN-
dc.subjectNEURODEGENERATION-
dc.subjectINJURY-
dc.subjectBRAIN-
dc.subjectAPOE-
dc.titleSynaptotagmin and synaptic transmission alterations in apolipoprotein E-deficient mice-
dc.typeArticle-
dc.identifier.wosid000080358600012-
dc.identifier.scopusid2-s2.0-0006237627-
dc.type.rimsART-
dc.citation.volume23-
dc.citation.issue3-
dc.citation.beginningpage519-
dc.citation.endingpage531-
dc.citation.publicationnamePROGRESS IN NEURO-PSYCHOPHARMACOLOGY BIOLOGICAL PSYCHIATRY-
dc.identifier.doi10.1016/S0278-5846(99)00013-5-
dc.contributor.localauthorJung, MW-
dc.contributor.nonIdAuthorVeinbergs, I-
dc.contributor.nonIdAuthorMante, M-
dc.contributor.nonIdAuthorVan Uden, E-
dc.contributor.nonIdAuthorMasliah, E-
dc.type.journalArticleReview-
dc.subject.keywordAuthorAlzheimer&apos-
dc.subject.keywordAuthors disease-
dc.subject.keywordAuthorapolipoprotein E-
dc.subject.keywordAuthorcalcium homeostasis-
dc.subject.keywordAuthorelectrophysiology-
dc.subject.keywordAuthorMorris water maze-
dc.subject.keywordAuthorsynaptotagmin.-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusCHOLINERGIC IMPAIRMENTS-
dc.subject.keywordPlusVESICLE PROTEIN-
dc.subject.keywordPlusNEURODEGENERATION-
dc.subject.keywordPlusINJURY-
dc.subject.keywordPlusBRAIN-
dc.subject.keywordPlusAPOE-
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