Document Type
Article
Publication Date
8-6-2018
Abstract
A-type voltage-gated potassium (Kv) channels are major regulators of neuronal excitability that have been mainly characterized in the central nervous system. By contrast, there is a paucity of knowledge about the molecular physiology of these Kv channels in the peripheral nervous system, including highly specialized and heterogenous dorsal root ganglion (DRG) neurons. Although all A-type Kv channels display pore-forming subunits with similar structural properties and fast inactivation, their voltage-, and time-dependent properties and modulation are significantly different. These differences ultimately determine distinct physiological roles of diverse A-type Kv channels, and how their dysfunction might contribute to neurological disorders. The importance of A-type Kv channels in DRG neurons is highlighted by recent studies that have linked their dysfunction to persistent pain sensitization. Here, we review the molecular neurophysiology of A-type Kv channels with an emphasis on those that have been identified and investigated in DRG nociceptors (Kv1.4, Kv3.4, and Kv4s). Also, we discuss evidence implicating these Kv channels in neuropathic pain resulting from injury, and present a perspective of outstanding challenges that must be tackled in order to discover novel treatments for intractable pain disorders.
Recommended Citation
Zemel, Benjamin M.; Ritter, David M.; Covarrubias, Manuel; and Muqeem, Tanziyah, "A-Type KV Channels in Dorsal Root Ganglion Neurons: Diversity, Function, and Dysfunction" (2018). Department of Neuroscience Faculty Papers. Paper 39.
https://jdc.jefferson.edu/department_neuroscience/39
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
Language
English
Comments
This article has been peer reviewed. It is the author’s final published version in Frontiers in Molecular Neuroscience by Frontiers Media, Volume 11, August 2018, Article number 253.
The published version is available at https://doi.org/10.3389/fnmol.2018.00253. Copyright © Zemel et al.