Knockout of the ASIC2 channel in mice does not impair cutaneous mechanosensation, visceral mechanonociception and hearing
- Carolina Roza2,
- Jean-Luc Puel4,
- Michaela Kress23,
- Anne Baron1,
- Sylvie Diochot1,
- Michel Lazdunski1 and
- Rainer Waldmann1
- 1Institut de Pharmacologie Moléculaire et Cellulaire, CNRS-UMR 6097, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France2Department of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremburg, Universitätsstrasse 17, D-91054 Erlangen, Germany3Department of Physiology, Fritz-Pregl-Strasse 3, A-6020 Innsbruck, Austria4INSERM U583, Physiopathologie et thérapie des déficits sensoriels et moteurs, 71 rue de Navacelles, 34090 Montpellier, France
- Corresponding author M. Lazdunski: Institut de Pharmacologie Moléculaire et Cellulaire, CNRS-UMR 6097, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France. Email: ipmc{at}ipmc.cnrs.fr
Abstract
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 neurones and are therefore interesting candidates for mammalian mechanosensors. We investigated the effect of an ASIC2 gene knockout in mice on hearing and on cutaneous mechanosensation and visceral mechanonociception. However, our data do not support a role of ASIC2 in those facets of mechanoperception.
Footnotes
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- Accepted May 28, 2004.
- Received April 6, 2004.
- Revision received May 24, 2004.
- The Physiological society 2004
