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Slack, Slick, and Sodium-Activated Potassium Channels

The Slack and Slick genes encode potassium channels that are very widely expressed in the central nervous system. These channels are activated by elevations in intracellular sodium, such as those that occur during trains of one or more action potentials, or following activation of nonselective catio...

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Autor principal: Kaczmarek, Leonard K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3850776/
https://www.ncbi.nlm.nih.gov/pubmed/24319675
http://dx.doi.org/10.1155/2013/354262
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author Kaczmarek, Leonard K.
author_facet Kaczmarek, Leonard K.
author_sort Kaczmarek, Leonard K.
collection PubMed
description The Slack and Slick genes encode potassium channels that are very widely expressed in the central nervous system. These channels are activated by elevations in intracellular sodium, such as those that occur during trains of one or more action potentials, or following activation of nonselective cationic neurotransmitter receptors such as AMPA receptors. This review covers the cellular and molecular properties of Slack and Slick channels and compares them with findings on the properties of sodium-activated potassium currents (termed K(Na) currents) in native neurons. Human mutations in Slack channels produce extremely severe defects in learning and development, suggesting that K(Na) channels play a central role in neuronal plasticity and intellectual function.
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spelling pubmed-38507762013-12-04 Slack, Slick, and Sodium-Activated Potassium Channels Kaczmarek, Leonard K. ISRN Neurosci Review Article The Slack and Slick genes encode potassium channels that are very widely expressed in the central nervous system. These channels are activated by elevations in intracellular sodium, such as those that occur during trains of one or more action potentials, or following activation of nonselective cationic neurotransmitter receptors such as AMPA receptors. This review covers the cellular and molecular properties of Slack and Slick channels and compares them with findings on the properties of sodium-activated potassium currents (termed K(Na) currents) in native neurons. Human mutations in Slack channels produce extremely severe defects in learning and development, suggesting that K(Na) channels play a central role in neuronal plasticity and intellectual function. Hindawi Publishing Corporation 2013-05-13 /pmc/articles/PMC3850776/ /pubmed/24319675 http://dx.doi.org/10.1155/2013/354262 Text en Copyright © 2013 Leonard K. Kaczmarek. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Kaczmarek, Leonard K.
Slack, Slick, and Sodium-Activated Potassium Channels
title Slack, Slick, and Sodium-Activated Potassium Channels
title_full Slack, Slick, and Sodium-Activated Potassium Channels
title_fullStr Slack, Slick, and Sodium-Activated Potassium Channels
title_full_unstemmed Slack, Slick, and Sodium-Activated Potassium Channels
title_short Slack, Slick, and Sodium-Activated Potassium Channels
title_sort slack, slick, and sodium-activated potassium channels
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3850776/
https://www.ncbi.nlm.nih.gov/pubmed/24319675
http://dx.doi.org/10.1155/2013/354262
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