Diminished KCC2 confounds synapse-specificity of LTP during senescence

Synapse-specificity of LTP ensures that no interference arises from inputs irrelevant to the memory to be encoded. In hippocampi of aged (21-28 months-old) mice LTP was relayed to unstimulated synapses blemishing its synapse-specificity. Diminished levels of the K(+)/Cl(–) cotransporter KCC2 and a d...

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Autores principales: Ferando, Isabella, Faas, Guido, Mody, Istvan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2016
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003660/
https://www.ncbi.nlm.nih.gov/pubmed/27500406
http://dx.doi.org/10.1038/nn.4357
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author Ferando, Isabella
Faas, Guido
Mody, Istvan
author_facet Ferando, Isabella
Faas, Guido
Mody, Istvan
author_sort Ferando, Isabella
collection PubMed
description Synapse-specificity of LTP ensures that no interference arises from inputs irrelevant to the memory to be encoded. In hippocampi of aged (21-28 months-old) mice LTP was relayed to unstimulated synapses blemishing its synapse-specificity. Diminished levels of the K(+)/Cl(–) cotransporter KCC2 and a depolarizing GABA(A) receptor-mediated synaptic component following LTP were the most likely causes for spreading the potentiation, unveiling novel mechanisms hindering information storage in the aged brain, and identifying KCC2 as a potential target for intervention.
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spelling pubmed-50036602017-02-08 Diminished KCC2 confounds synapse-specificity of LTP during senescence Ferando, Isabella Faas, Guido Mody, Istvan Nat Neurosci Article Synapse-specificity of LTP ensures that no interference arises from inputs irrelevant to the memory to be encoded. In hippocampi of aged (21-28 months-old) mice LTP was relayed to unstimulated synapses blemishing its synapse-specificity. Diminished levels of the K(+)/Cl(–) cotransporter KCC2 and a depolarizing GABA(A) receptor-mediated synaptic component following LTP were the most likely causes for spreading the potentiation, unveiling novel mechanisms hindering information storage in the aged brain, and identifying KCC2 as a potential target for intervention. 2016-08-08 2016-09 /pmc/articles/PMC5003660/ /pubmed/27500406 http://dx.doi.org/10.1038/nn.4357 Text en Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Ferando, Isabella
Faas, Guido
Mody, Istvan
Diminished KCC2 confounds synapse-specificity of LTP during senescence
title Diminished KCC2 confounds synapse-specificity of LTP during senescence
title_full Diminished KCC2 confounds synapse-specificity of LTP during senescence
title_fullStr Diminished KCC2 confounds synapse-specificity of LTP during senescence
title_full_unstemmed Diminished KCC2 confounds synapse-specificity of LTP during senescence
title_short Diminished KCC2 confounds synapse-specificity of LTP during senescence
title_sort diminished kcc2 confounds synapse-specificity of ltp during senescence
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003660/
https://www.ncbi.nlm.nih.gov/pubmed/27500406
http://dx.doi.org/10.1038/nn.4357
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