Heteromultimers of DEG/ENaC subunits form H+-gated channels in mouse sensory neurons

Christopher J Benson; Jinghui Xie; John A Wemmie; Margaret P Price; Jillian M Henss; Michael J Welsh; Peter M Snyder

doi:10.1073/pnas.032678399

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Heteromultimers of DEG/ENaC subunits form H+-gated channels in mouse sensory neurons

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Heteromultimers of DEG/ENaC subunits form H+-gated channels in mouse sensory neurons

Christopher J Benson, Jinghui Xie, John A Wemmie, Margaret P Price, Jillian M Henss, Michael J Welsh and Peter M Snyder

Proceedings of the National Academy of Sciences - PNAS, Vol.99(4), pp.2338-2343

02/19/2002

DOI: 10.1073/pnas.032678399

PMCID: PMC122366

PMID: 11854527

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Abstract

Acidic extracellular solution activates transient H + -gated currents in dorsal root ganglion (DRG) neurons. The biophysical properties of three degenerin/epithelial sodium (DEG/ENaC) channel subunits (BNC1, ASIC, and DRASIC), and their expression in DRG, suggest that they might underlie these H + -gated currents and function as sensory transducers. However, it is uncertain which of these DEG/ENaC subunits generate the currents, and whether they function as homomultimers or heteromultimers. We found that the biophysical properties of transient H + -gated currents from medium to large mouse DRG neurons differed from BNC1, ASIC, or DRASIC expressed individually, but were reproduced by coexpression of the subunits together. To test the contribution of each subunit, we studied DRG from three strains of mice, each bearing a targeted disruption of BNC1, ASIC, or DRASIC. Deletion of any one subunit did not abolish H + -gated currents, but altered currents in a manner consistent with heteromultimerization of the two remaining subunits. These data indicate that combinations of two or more DEG/ENaC subunits coassemble as heteromultimers to generate transient H + -gated currents in mouse DRG neurons.

Biological Sciences

Details

Title: Subtitle: Heteromultimers of DEG/ENaC subunits form H+-gated channels in mouse sensory neurons
Creators: Christopher J Benson - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
Jinghui Xie - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
John A Wemmie - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
Margaret P Price - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
Jillian M Henss - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
Michael J Welsh - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
Peter M Snyder - Howard Hughes Medical Institute, University of Iowa College of Medicine, Iowa City, IA 52242
Resource Type: Journal article
Publication Details: Proceedings of the National Academy of Sciences - PNAS, Vol.99(4), pp.2338-2343
DOI: 10.1073/pnas.032678399
PMID: 11854527
PMCID: PMC122366
NLM abbreviation: Proc Natl Acad Sci U S A
ISSN: 0027-8424
eISSN: 1091-6490
Publisher: National Academy of Sciences
Language: English
Date published: 02/19/2002
Academic Unit: Neurology; Molecular Physiology and Biophysics; Psychiatry; Iowa Neuroscience Institute; Neuroscience and Pharmacology; Neurosurgery; Medicine Administration; Internal Medicine
Record Identifier: 9984003989902771

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