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Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit

The electrogenic machinery of an excitable cell can adapt in response to changes in input, genetic deficit or in pathological conditions, however the underlying molecular mechanisms are not understood. In cases of genetic deletion it is commonly observed that a channel subunit from the same family r...

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Autor principal: Tabarean, Iustin V.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4010509/
https://www.ncbi.nlm.nih.gov/pubmed/24797243
http://dx.doi.org/10.1371/journal.pone.0096643
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author Tabarean, Iustin V.
author_facet Tabarean, Iustin V.
author_sort Tabarean, Iustin V.
collection PubMed
description The electrogenic machinery of an excitable cell can adapt in response to changes in input, genetic deficit or in pathological conditions, however the underlying molecular mechanisms are not understood. In cases of genetic deletion it is commonly observed that a channel subunit from the same family replaces the missing one. We have previously reported that Kv4.2−/− preoptic GABAergic neurons display identical firing characteristics to those of wild-type neurons despite having reduced A-type currents, and that, surprisingly, they present a robust upregulation of a delayed rectifier current, the nature of which is unknown. Here, using pharmacology, qPCR and Western blots we report that, although the wild-type neurons express several Kv subunits, the upregulated current is conducted by the Kv1.5 subunit exclusively. Thus, this study reveals the molecular nature of a novel mechanism of electrical remodeling in central neurons.
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spelling pubmed-40105092014-05-09 Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit Tabarean, Iustin V. PLoS One Research Article The electrogenic machinery of an excitable cell can adapt in response to changes in input, genetic deficit or in pathological conditions, however the underlying molecular mechanisms are not understood. In cases of genetic deletion it is commonly observed that a channel subunit from the same family replaces the missing one. We have previously reported that Kv4.2−/− preoptic GABAergic neurons display identical firing characteristics to those of wild-type neurons despite having reduced A-type currents, and that, surprisingly, they present a robust upregulation of a delayed rectifier current, the nature of which is unknown. Here, using pharmacology, qPCR and Western blots we report that, although the wild-type neurons express several Kv subunits, the upregulated current is conducted by the Kv1.5 subunit exclusively. Thus, this study reveals the molecular nature of a novel mechanism of electrical remodeling in central neurons. Public Library of Science 2014-05-05 /pmc/articles/PMC4010509/ /pubmed/24797243 http://dx.doi.org/10.1371/journal.pone.0096643 Text en © 2014 Iustin V http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Tabarean, Iustin V.
Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit
title Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit
title_full Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit
title_fullStr Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit
title_full_unstemmed Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit
title_short Electrical Remodeling of Preoptic GABAergic Neurons Involves the Kv1.5 Subunit
title_sort electrical remodeling of preoptic gabaergic neurons involves the kv1.5 subunit
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4010509/
https://www.ncbi.nlm.nih.gov/pubmed/24797243
http://dx.doi.org/10.1371/journal.pone.0096643
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