Papers

Peer-reviewed
May, 2011

Sour Taste Responses in Mice Lacking PKD Channels

PLOS ONE
  • Nao Horio
  • ,
  • Ryusuke Yoshida
  • ,
  • Keiko Yasumatsu
  • ,
  • Yuchio Yanagawa
  • ,
  • Yoshiro Ishimaru
  • ,
  • Hiroaki Matsunami
  • ,
  • Yuzo Ninomiya

Volume
6
Number
5
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1371/journal.pone.0020007
Publisher
PUBLIC LIBRARY SCIENCE

Background: The polycystic kidney disease-like ion channel PKD2L1 and its associated partner PKD1L3 are potential candidates for sour taste receptors. PKD2L1 is expressed in type III taste cells that respond to sour stimuli and genetic elimination of cells expressing PKD2L1 substantially reduces chorda tympani nerve responses to sour taste stimuli. However, the contribution of PKD2L1 and PKD1L3 to sour taste responses remains unclear.
Methodology/Principal Findings: We made mice lacking PKD2L1 and/or PKD1L3 gene and investigated whole nerve responses to taste stimuli in the chorda tympani or the glossopharyngeal nerve and taste responses in type III taste cells. In mice lacking PKD2L1 gene, chorda tympani nerve responses to sour, but not sweet, salty, bitter, and umami tastants were reduced by 25-45% compared with those in wild type mice. In contrast, chorda tympani nerve responses in PKD1L3 knockout mice and glossopharyngeal nerve responses in single-and double-knock-out mice were similar to those in wild type mice. Sour taste responses of type III fungiform taste cells (GAD67-expressing taste cells) were also reduced by 25-45% by elimination of PKD2L1.
Conclusions/Significance: These findings suggest that PKD2L1 partly contributes to sour taste responses in mice and that receptors other than PKDs would be involved in sour detection.

Link information
DOI
https://doi.org/10.1371/journal.pone.0020007
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000290771200039&DestApp=WOS_CPL
ID information
  • DOI : 10.1371/journal.pone.0020007
  • ISSN : 1932-6203
  • Web of Science ID : WOS:000290771200039

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