Title
<tex>$K{v}3$</tex> channels contribute to the delayed rectifier current in small cultured mouse dorsal root ganglion neurons <tex>$K{v}3$</tex> channels contribute to the delayed rectifier current in small cultured mouse dorsal root ganglion neurons
Author
Faculty/Department
Faculty of Medicine and Health Sciences
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Publication type
article
Publication
Bethesda, Md ,
Subject
Biology
Human medicine
Source (journal)
American journal of physiology: cell physiology. - Bethesda, Md
Volume/pages
303(2012) :4 , p. C406-C415
ISSN
0363-6143
ISI
000307804800007
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
fBocksteins E, Van de Vijver G, Van Bogaert PP, Snyders DJ. K(V)3 channels contribute to the delayed rectifier current in small cultured mouse dorsal root ganglion neurons. Am J Physiol Cell Physiol 303: C406-C415, 2012. First published June 6, 2012; doi:10.1152/ajpcell.00343.2011.-Delayed rectifier voltage-gated K+ (K-V) channels are important determinants of neuronal excitability. However, the large number of K-V subunits poses a major challenge to establish the molecular composition of the native neuronal K+ currents. A large part (similar to 60%) of the delayed rectifier current (I-K) in small mouse dorsal root ganglion (DRG) neurons has been shown to be carried by both homotetrameric K(V)2.1 and heterotetrameric channels of K(V)2 subunits with silent K-V subunits (KVS), while a contribution of K(V)1 channels has also been demonstrated. Because K(V)3 subunits also generate delayed rectifier currents, we investigated the contribution of K(V)3 subunits to I-K in small mouse DRG neurons. After stromatoxin (ScTx) pretreatment to block the K(V)2-containing component, application of 1 mM TEA caused significant additional block, indicating that the ScTx-insensitive part of I-K could include K(V)1, K(V)3, and/or M-current channels (KCNQ2/3). Combining ScTx and dendrotoxin confirmed a relevant contribution of K(V)2 and K(V)2/KVS, and K(V)1 subunits to I-K in small mouse DRG neurons. After application of these toxins, a significant TEA-sensitive current (similar to 19% of total I-K) remained with biophysical properties that corresponded to those of K(V)3 currents obtained in expression systems. Using RT-PCR, we detected K(V)3.1-3 mRNA in DRG neurons. Furthermore, Western blot and immunocytochemistry using K(V)3.1-specific antibodies confirmed the presence of K(V)3.1 in cultured DRG neurons. These biophysical, pharmacological, and molecular results demonstrate a relevant contribution (similar to 19%) of K(V)3-containing channels to I-K in small mouse DRG neurons, supporting a substantial role for K(V)3 subunits in these neurons.
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