Dopaminergic neurotransmission dysfunction induced by amyloid-? transforms cortical long-term potentiation into long-term depression and produces memory impairment

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dc.audience researchers es_MX
dc.contributor.author Kioko Guzmán-Ramos, 0000-0002-5180-4127
dc.contributor.author Federico Bermudez_Rattoni, 0000-0003-2056-6119
dc.contributor.other Moreno Castilla, Perla
dc.contributor.other Rodriguez Durán, Luis F.
dc.contributor.other Bárcenas Femat, Alejandro
dc.contributor.other Escobar, Martha L.
dc.coverage MX es_MX
dc.date.accessioned 2018-06-27T01:08:28Z
dc.date.available 2018-06-27T01:08:28Z
dc.date.issued 2016
dc.description Alzheimer'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.format application/pdf es_MX
dc.identificador.materia 3 es_MX
dc.identifier.uri http://hdl.handle.net/20.500.12222/165
dc.language eng es_MX
dc.publisher Universidad Autónoma Metropolitana. Unidad Lerma es_MX
dc.rights Attribution-NonCommercial-NoDerivatives 4.0 Internacional *
dc.rights.license info:eu-repo/semantics/openAccess es_MX
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/4.0/ es_MX
dc.subject MEDICINA Y CIENCIAS DE LA SALUD es_MX
dc.subject.keywords Amyloid-beta es_MX
dc.subject.keywords Alzheimer's disease es_MX
dc.subject.keywords Long-term depression es_MX
dc.subject.keywords Long-term potentiation es_MX
dc.subject.keywords Dopamine es_MX
dc.subject.keywords Recognition memory impairment es_MX
dc.title Dopaminergic neurotransmission dysfunction induced by amyloid-? transforms cortical long-term potentiation into long-term depression and produces memory impairment es_MX
dc.type preprint es_MX
dc.type.version info:eu-repo/semantics/publishedVersion es_MX
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