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ISRN Neuroscience
Volume 2013 (2013), Article ID 354262, 14 pages
http://dx.doi.org/10.1155/2013/354262
Review Article

Slack, Slick, and Sodium-Activated Potassium Channels

Departments of Pharmacology and Cellular and Molecular Physiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8066, USA

Received 24 February 2013; Accepted 18 April 2013

Academic Editors: Y. Bozzi, A. Kulik, and W. Van Drongelen

Copyright © 2013 Leonard K. Kaczmarek. 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.

Abstract

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 KNa currents) in native neurons. Human mutations in Slack channels produce extremely severe defects in learning and development, suggesting that KNa channels play a central role in neuronal plasticity and intellectual function.