RRC ID 6340
Author Cai SQ, Sesti F.
Title Oxidation of a potassium channel causes progressive sensory function loss during aging.
Journal Nat Neurosci
Abstract Potassium channels are key regulators of neuronal excitability. Here we show that oxidation of the K(+) channel KVS-1 during aging causes sensory function loss in Caenorhabditis elegans and that protection of this channel from oxidation preserves neuronal function. Chemotaxis, a function controlled by KVS-1, was significantly impaired in worms exposed to oxidizing agents, but only moderately affected in worms harboring an oxidation-resistant KVS-1 mutant (C113S). In aging C113S transgenic worms, the effects of free radical accumulation were significantly attenuated compared to those in wild type. Electrophysiological analyses showed that both reactive oxygen species (ROS) accumulation during aging and acute exposure to oxidizing agents acted primarily to alter the excitability of the neurons that mediate chemotaxis. Together, these findings establish a pivotal role for ROS-mediated oxidation of voltage-gated K(+) channels in sensorial decline during aging in invertebrates.
Volume 12(5)
Pages 611-7
Published 2009-5-1
DOI 10.1038/nn.2291
PII nn.2291
PMID 19330004
PMC PMC2685168
MeSH Action Potentials / physiology Animals Animals, Genetically Modified CHO Cells Caenorhabditis elegans / cytology Caenorhabditis elegans / genetics Caenorhabditis elegans / metabolism* Caenorhabditis elegans Proteins / genetics Caenorhabditis elegans Proteins / metabolism* Chemotaxis / physiology Cricetinae Cricetulus Free Radicals / metabolism Nervous System / cytology Nervous System / metabolism* Oxidative Stress / physiology* Potassium Channels, Voltage-Gated / genetics Potassium Channels, Voltage-Gated / metabolism* Reactive Oxygen Species / metabolism Sensation Disorders / genetics Sensation Disorders / metabolism* Sensation Disorders / physiopathology Sensory Receptor Cells / metabolism
IF 20.071
Times Cited 45
WOS Category NEUROSCIENCES
Resource
C.elegans tm2034