CaMKII inhibitor 1 (CaMK2N1) mRNA is upregulated following LTP induction in hippocampal slices
Author
dc.contributor.author
Astudillo Maya, Andrea
Author
dc.contributor.author
Karmelic Visinteiner, Daniel
Author
dc.contributor.author
Casas Atala, Bárbara
Author
dc.contributor.author
Otmakhov, Nikolai
Author
dc.contributor.author
Palma Alvarado, Verónica
Author
dc.contributor.author
Sanhueza Toha, María Magdalena
Admission date
dc.date.accessioned
2020-06-23T20:58:00Z
Available date
dc.date.available
2020-06-23T20:58:00Z
Publication date
dc.date.issued
2020
Cita de ítem
dc.identifier.citation
Synapse 2020;00:e22158
es_ES
Identifier
dc.identifier.other
10.1002/syn.22158
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/175652
Abstract
dc.description.abstract
CaMK2N1 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
Patrocinador
dc.description.sponsorship
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDECYT
1140700
United States Department of Health & Human Services
National Institutes of Health (NIH) - USA
R01NS103168
R01DA043195