Format

Send to

Choose Destination
See comment in PubMed Commons below
Neuron. 2011 Sep 8;71(5):845-57. doi: 10.1016/j.neuron.2011.06.038.

DEG/ENaC but not TRP channels are the major mechanoelectrical transduction channels in a C. elegans nociceptor.

Author information

1
Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA.

Abstract

Many nociceptors detect mechanical cues, but the ion channels responsible for mechanotransduction in these sensory neurons remain obscure. Using in vivo recordings and genetic dissection, we identified the DEG/ENaC protein, DEG-1, as the major mechanotransduction channel in ASH, a polymodal nociceptor in Caenorhabditis elegans. But DEG-1 is not the only mechanotransduction channel in ASH: loss of deg-1 revealed a minor current whose properties differ from those expected of DEG/ENaC channels. This current was independent of two TRPV channels expressed in ASH. Although loss of these TRPV channels inhibits behavioral responses to noxious stimuli, we found that both mechanoreceptor currents and potentials were essentially wild-type in TRPV mutants. We propose that ASH nociceptors rely on two genetically distinct mechanotransduction channels and that TRPV channels contribute to encoding and transmitting information. Because mammalian and insect nociceptors also coexpress DEG/ENaCs and TRPVs, the cellular functions elaborated here for these ion channels may be conserved.

PMID:
21903078
PMCID:
PMC3170654
DOI:
10.1016/j.neuron.2011.06.038
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center