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Chemical Senses Advance Access originally published online on August 31, 2005
Chemical Senses 2005 30(7):593-600; doi:10.1093/chemse/bji053
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

PLCß2-Independent Behavioral Avoidance of Prototypical Bitter-Tasting Ligands

Cedrick D. Dotson1, Stephen D. Roper2 and Alan C. Spector1

1 Department of Psychology and Center for Smell and Taste, University of Florida, Gainesville, FL 32611-2250, USA and 2 Department of Physiology and Biophysics, and Neuroscience Program, University of Miami School of Medicine, 1600 NW 10th Avenue, Miami, FL 33136, USA

Correspondence to be sent to: Alan C. Spector, Department of Psychology, University of Florida, PO Box 112250, Gainesville, FL 32611-2250, USA. e-mail: spector{at}ufl.edu

Using a brief-access taste assay, we show in the present report that although phospholipase C ß2 knockout (PLCß2 KO) mice are unresponsive to low- and midrange concentrations of quinine and denatonium, they do significantly avoid licking higher concentrations of these aversive compounds. PLCß2 KO mice displayed no concentration-dependent licking of the prototypical sweetener sucrose but were similar to wild-type mice in their responses to citric acid and NaCl, notwithstanding some interesting exceptions. Although these findings confirm an essential role for PLCß2 in taste responsiveness to sucrose and to low- to midrange concentrations of quinine and denatonium in mice as previously reported, they importantly suggest that higher concentrations of the latter two compounds, which are bitter to humans, can engage a PLCß2-independent taste transduction pathway.

Key words: licking, mice, phosphoinositide signaling, taste transduction, T1R, T2R


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