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The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons

Delayed rectifier voltage‐gated K(+) (Kv) channels play an important role in the regulation of the electrophysiological properties of neurons. In mouse dorsal root ganglion (DRG) neurons, a large fraction of the delayed rectifier current is carried by both homotetrameric Kv2 channels and heterotetra...

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Autores principales: Regnier, Glenn, Bocksteins, Elke, Van de Vijver, Gerda, Snyders, Dirk J., van Bogaert, Pierre‐Paul
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4814888/
https://www.ncbi.nlm.nih.gov/pubmed/27033450
http://dx.doi.org/10.14814/phy2.12731
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author Regnier, Glenn
Bocksteins, Elke
Van de Vijver, Gerda
Snyders, Dirk J.
van Bogaert, Pierre‐Paul
author_facet Regnier, Glenn
Bocksteins, Elke
Van de Vijver, Gerda
Snyders, Dirk J.
van Bogaert, Pierre‐Paul
author_sort Regnier, Glenn
collection PubMed
description Delayed rectifier voltage‐gated K(+) (Kv) channels play an important role in the regulation of the electrophysiological properties of neurons. In mouse dorsal root ganglion (DRG) neurons, a large fraction of the delayed rectifier current is carried by both homotetrameric Kv2 channels and heterotetrameric channels consisting of Kv2 and silent Kv (KvS) subunits (i.e., Kv5‐Kv6 and Kv8‐Kv9). However, little is known about the contribution of Kv2‐mediated currents during the postnatal development of DRG neurons. Here, we report that the Stromatoxin‐1 (ScTx)‐sensitive fraction of the total outward K(+) current (I(K)) from mouse DRG neurons gradually decreased (~13%, P < 0.05) during the first month of postnatal development. Because ScTx inhibits both Kv2.1‐ and Kv2.2‐mediated currents, this gradual decrease may reflect a decrease in currents containing either subunit. However, the fraction of Kv2.1 antibody‐sensitive current that only reflects the Kv2.1‐mediated currents remained constant during that same period. These results suggested that the fractional contribution of Kv2.2‐mediated currents relative to I(K) decreased with postnatal age. Semiquantitative RT‐PCR analysis indicated that this decrease can be attributed to developmental changes in Kv2.2 expression as the mRNA levels of the Kv2.2 subunit decreased gradually between 1 and 4 weeks of age. In addition, we observed age‐dependent fluctuations in the mRNA levels of the Kv6.3, Kv8.1, Kv9.1, and Kv9.3 subunits. These results support an important role of both Kv2 and KvS subunits in the postnatal maturation of DRG neurons.
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spelling pubmed-48148882016-04-11 The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons Regnier, Glenn Bocksteins, Elke Van de Vijver, Gerda Snyders, Dirk J. van Bogaert, Pierre‐Paul Physiol Rep Original Research Delayed rectifier voltage‐gated K(+) (Kv) channels play an important role in the regulation of the electrophysiological properties of neurons. In mouse dorsal root ganglion (DRG) neurons, a large fraction of the delayed rectifier current is carried by both homotetrameric Kv2 channels and heterotetrameric channels consisting of Kv2 and silent Kv (KvS) subunits (i.e., Kv5‐Kv6 and Kv8‐Kv9). However, little is known about the contribution of Kv2‐mediated currents during the postnatal development of DRG neurons. Here, we report that the Stromatoxin‐1 (ScTx)‐sensitive fraction of the total outward K(+) current (I(K)) from mouse DRG neurons gradually decreased (~13%, P < 0.05) during the first month of postnatal development. Because ScTx inhibits both Kv2.1‐ and Kv2.2‐mediated currents, this gradual decrease may reflect a decrease in currents containing either subunit. However, the fraction of Kv2.1 antibody‐sensitive current that only reflects the Kv2.1‐mediated currents remained constant during that same period. These results suggested that the fractional contribution of Kv2.2‐mediated currents relative to I(K) decreased with postnatal age. Semiquantitative RT‐PCR analysis indicated that this decrease can be attributed to developmental changes in Kv2.2 expression as the mRNA levels of the Kv2.2 subunit decreased gradually between 1 and 4 weeks of age. In addition, we observed age‐dependent fluctuations in the mRNA levels of the Kv6.3, Kv8.1, Kv9.1, and Kv9.3 subunits. These results support an important role of both Kv2 and KvS subunits in the postnatal maturation of DRG neurons. John Wiley and Sons Inc. 2016-03-31 /pmc/articles/PMC4814888/ /pubmed/27033450 http://dx.doi.org/10.14814/phy2.12731 Text en © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Regnier, Glenn
Bocksteins, Elke
Van de Vijver, Gerda
Snyders, Dirk J.
van Bogaert, Pierre‐Paul
The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
title The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
title_full The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
title_fullStr The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
title_full_unstemmed The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
title_short The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
title_sort contribution of kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4814888/
https://www.ncbi.nlm.nih.gov/pubmed/27033450
http://dx.doi.org/10.14814/phy2.12731
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