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Knockout of the ASIC2 channel in mice does not impair cutaneous mechanosensation, visceral mechanonociception and hearing
Author(s) -
Roza Carolina,
Puel JeanLuc,
Kress Michaela,
Baron Anne,
Diochot Sylvie,
Lazdunski Michel,
Waldmann Rainer
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.066001
Subject(s) - mechanosensation , mechanosensitive channels , knockout mouse , acid sensing ion channel , mechanotransduction , ion channel , piezo1 , sensory system , epithelial sodium channel , biology , microbiology and biotechnology , neuroscience , chemistry , gene , genetics , receptor , organic chemistry , sodium
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.