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dc.contributor.authorKioko Guzmán-Ramos, 0000-0002-5180-4127-
dc.contributor.authorFederico Bermudez_Rattoni, 0000-0003-2056-6119-
dc.contributor.otherMoreno Castilla, Perla-
dc.contributor.otherRodriguez Durán, Luis F.-
dc.contributor.otherBárcenas Femat, Alejandro-
dc.contributor.otherEscobar, Martha L.-
dc.date.accessioned2018-06-27T01:08:28Z-
dc.date.available2018-06-27T01:08:28Z-
dc.date.issued2016-
dc.identifier.urihttp://hdl.handle.net/20.500.12222/165-
dc.descriptionAlzheimer's disease (AD) is a neurodegenerative condition manifested by synaptic dysfunction and memory loss, but the mechanisms underlying synaptic failure are not entirely understood. Although dopamine is a key modulator of synaptic plasticity, dopaminergic neurotransmission dysfunction in AD has mostly been associated to noncognitive symptoms. Thus, we aimed to study the relationship between dopaminergic neurotransmission and synaptic plasticity in AD models. We used a transgenic model of AD (triple-transgenic mouse model of AD) and the administration of exogenous amyloid-β (Aβ) oligomers into wild type mice. We found that Aβ decreased cortical dopamine levels and converted in vivo long-term potentiation (LTP) into long-term depression (LTD) after high-frequency stimulation delivered at basolateral amygdaloid nucleus–insular cortex projection, which led to impaired recognition memory. Remarkably, increasing cortical dopamine and norepinephrine levels rescued both high-frequency stimulation -induced LTP and memory, whereas depletion of catecholaminergic levels mimicked the Aβ-induced shift from LTP to LTD. Our results suggest that Aβ-induced dopamine depletion is a core mechanism underlying the early synaptopathy and memory alterations observed in AD models and acts by modifying the threshold for the induction of cortical LTP and/or LTD.es_MX
dc.formatapplication/pdfes_MX
dc.languageenges_MX
dc.publisherUniversidad Autónoma Metropolitana. Unidad Lermaes_MX
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/es_MX
dc.subjectMEDICINA Y CIENCIAS DE LA SALUDes_MX
dc.titleDopaminergic neurotransmission dysfunction induced by amyloid-? transforms cortical long-term potentiation into long-term depression and produces memory impairmentes_MX
dc.typepreprintes_MX
dc.rights.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.rights.licenseinfo:eu-repo/semantics/openAccesses_MX
dc.subject.keywordsAmyloid-betaes_MX
dc.subject.keywordsAlzheimer's diseasees_MX
dc.subject.keywordsLong-term depressiones_MX
dc.subject.keywordsLong-term potentiationes_MX
dc.subject.keywordsDopaminees_MX
dc.subject.keywordsRecognition memory impairmentes_MX
dc.type.versioninfo:eu-repo/semantics/publishedVersiones_MX
dc.coverageMXes_MX
dc.audienceresearcherses_MX
dc.identificador.materia3es_MX
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