Pharmacological Modulation of Three Modalities of CA1 Hippocampal Long-Term Potentiation in the Ts65Dn Mouse Model of Down Syndrome

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dc.contributor.authorScott-McKean, Jonah J.
dc.contributor.authorRoque, Adriano L. [UNIFESP]
dc.contributor.authorSurewicz, Krystyna
dc.contributor.authorJohnson, Mark W.
dc.contributor.authorSurewicz, Witold K.
dc.contributor.authorCosta, Alberto C. S.
dc.coverageLondon
dc.date.accessioned2020-07-02T18:51:51Z
dc.date.available2020-07-02T18:51:51Z
dc.date.issued2018
dc.description.abstractThe Ts65Dn mouse is the most studied animal model of Down syndrome. Past research has shown a significant reduction in CA1 hippocampal long-term potentiation (LTP) induced by theta-burst stimulation (TBS), but not in LTP induced by high-frequency stimulation (HFS), in slices from Ts65Dn mice compared with euploid mouse-derived slices. Additionally, therapeutically relevant doses of the drug memantine were shown to rescue learning and memory deficits in Ts65Dn mice. Here, we observed that 1 mu M memantine had no detectable effect on HFS-induced LTP in either Ts65Dn- or control-derived slices, but it rescued TBS-induced LTP in Ts65Dn-derived slices to control euploid levels. Then, we assessed LTP induced by four HFS (4xHFS) and found that this form of LTP was significantly depressed in Ts65Dn slices when compared with LTP in euploid control slices. Memantine, however, did not rescue this phenotype. Because 4xHFS-induced LTP had not yet been characterized in Ts65Dn mice, we also investigated the effects of picrotoxin, amyloid beta oligomers, and soluble recombinant human prion protein (rPrP) on this form of LTP. Whereas >= 10 mu M picrotoxin increased LTP to control levels, it also caused seizure-like oscillations. Neither amyloid beta oligomers nor rPrP had any effect on 4xHFS-induced LTP in Ts65Dn-derived slices.en
dc.description.affiliationCase Western Reserve Univ, Dept Pediat, Div Pediat Neurol, Cleveland, OH 44106 USA
dc.description.affiliationUniv Fed Sao Paulo, Cardiol, Postgrad Program Med, BR-04024002 Sao Paulo, SP, Brazil
dc.description.affiliationCase Western Reserve Univ, Dept Physiol & Biophys, Cleveland, OH 44106 USA
dc.description.affiliationCase Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA
dc.description.affiliationUnifespUniv Fed Sao Paulo, Cardiol, Postgrad Program Med, BR-04024002 Sao Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipAlana USA Foundation [124124]
dc.description.sponsorshipCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
dc.description.sponsorshipAwakening Angels
dc.description.sponsorshipNIH [NS083687]
dc.description.sponsorshipIDCAPES: NS083687
dc.format.extent-
dc.identifierhttp://dx.doi.org/10.1155/2018/9235796
dc.identifier.citationNeural Plasticity. London, v. , p. -, 2018.
dc.identifier.doi10.1155/2018/9235796
dc.identifier.fileWOS000430694600001.pdf
dc.identifier.issn2090-5904
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/53754
dc.identifier.wosWOS:000430694600001
dc.language.isoeng
dc.publisherHindawi Ltd
dc.relation.ispartofNeural Plasticity
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titlePharmacological Modulation of Three Modalities of CA1 Hippocampal Long-Term Potentiation in the Ts65Dn Mouse Model of Down Syndromeen
dc.typeinfo:eu-repo/semantics/article
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