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Authordc.contributor.authorAstudillo Maya, Andrea 
Authordc.contributor.authorKarmelic Visinteiner, Daniel 
Authordc.contributor.authorCasas Atala, Bárbara 
Authordc.contributor.authorOtmakhov, Nikolai 
Authordc.contributor.authorPalma Alvarado, Verónica 
Authordc.contributor.authorSanhueza Toha, María Magdalena 
Admission datedc.date.accessioned2020-06-23T20:58:00Z
Available datedc.date.available2020-06-23T20:58:00Z
Publication datedc.date.issued2020
Cita de ítemdc.identifier.citationSynapse 2020;00:e22158es_ES
Identifierdc.identifier.other10.1002/syn.22158
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/175652
Abstractdc.description.abstractCaMK2N1 and CaMK2N2 (also known as CaMKIIN alpha and beta) are endogenous inhibitors of calcium/calmodulin-dependent kinase II (CaMKII), an enzyme critical for memory and long-term potentiation (LTP), a form of synaptic plasticity thought to underlie learning. CaMK2N1/2 mRNAs are rapidly and differentially upregulated in the hippocampus and amygdala after acquisition or retrieval of fear memory. Moreover, CaMK2N2 protein levels increase after contextual fear conditioning. Therefore, it was proposed that CaMK2N1/2 genes (Camk2n1/2) could be immediate-early genes transcribed promptly (30-60 min) after training. As a first approach to explore a role in synaptic plasticity, we assessed a possible regulation of Camk2n1/2 during the expression phase of LTP in hippocampal CA3-CA1 connections in rat brain slices. Quantitative PCR revealed that Camk2n1, but not Camk2n2, is upregulated 60 min after LTP induction by Schaffer collaterals high-frequency stimulation. We observed a graded, significant positive correlation between the magnitude of LTP and Camk2n1 change in individual slices, suggesting a coordinated regulation of these properties. If mRNA increment actually resulted in the protein upregulation in plasticity-relevant subcellular locations, CaMK2N1 may be involved in CaMKII fine-tuning during LTP maintenance or in the regulation of subsequent plasticity events (metaplasticity).es_ES
Patrocinadordc.description.sponsorshipComision Nacional de Investigacion Cientifica y Tecnologica (CONICYT) CONICYT FONDECYT 1140700 United States Department of Health & Human Services National Institutes of Health (NIH) - USA R01NS103168 R01DA043195es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherWileyes_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceSynapsees_ES
Keywordsdc.subjectCaMKIIes_ES
Keywordsdc.subjectGene expressiones_ES
Keywordsdc.subjectLTPes_ES
Títulodc.titleCaMKII inhibitor 1 (CaMK2N1) mRNA is upregulated following LTP induction in hippocampal sliceses_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadorapces_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile