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First published online on May 28, 2004.
 Copyright © 2004 by The Physiological Society
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jphysiol.2004.066001v1
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Received April 6, 2004
Revised May 10, 2004
Accepted after revision May 24, 2004

Knockout of the ASIC2 channel does not impair cutaneous mechanosensation, visceral mechanonociception and hearing

Carolina Roza1, Jean- Luc Puel2, Michaela Kress3, Anne Baron4, Sylvie Diochot4, Michel Lazdunski4*, and Rainer Waldmann4

1 Department of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremberg, Germany
2 Physiopathologie et thérapie des déficits sensoriels et moteurs, Inserm U538, France
3 Department of Physiology, Fritz-Pregl-Str. 3, A-6020 Innsbruck, Austria
4 Institut de Pharmacologie Moléculaire et Cellulaire, CNRS-UMR 6097, France

* To whom correspondence should be addressed. E-mail: lazdunski{at}ipmc.cnrs.fr.

Mechanosensitive cation channels are thought to be crucial for different aspects of mechanoperception such as hearing and touch sensation. In the nematode C. elegans, the degenerins MEC-4 and MEC-10 are involved in mechanosensation and were proposed to form mechanosensitive cation channels. Mammalian degenerin homologues, the H+ gated ASIC channels, are expressed in sensory neurons and are thus interesting candidates for mammalian mechanosensors. We investigated the effect of an ASIC2 gene knockout on hearing and on cutaneous mechanosensation and visceral mechanonociception. However, our data do not support a role of ASIC2 in those facets of mechanoperception.


Key words: Ion channel • Mechanosensitivity • Nociception






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