Rapid kinetics of second messenger production in bitter taste.
Spielman, Andrew I., Hajime Nagai, Gulshan Sunavala, Maximillian
Dasso, Heinz Breer, Ingrid Boekhoff, Taufiqul Huque, Glayde Whitney,
and Joseph G. Brand.
Basic Science Division, New York University College of Dentistry,
New York, NY 10010; Tel: (212) 998-9564, Fax (212) 995-4087, Monell
Chemical Senses Center, 3500 Market Street, Philadelphia, PA 19104;
University Stuttgart-Hohenheim, Dept. of Zoophysiology, 7000
Stuttgart 70, Germany; Dept. of Biochemistry, School of Dental
Medicine, University of Pennsylvania, and the Veterans Affairs
Medical Center, Philadelphia, PA 19104; Institute for Fundamental
Research, Suntory Limited, Osaka, Japan; Dept. of Psychology, Florida
State University, Tallahassee, FL
APStracts 2:0398C, 1995.
Tasting of bitter compounds may have evolved as a protective mechanism
against ingestion of potentially harmful substances. We have
identified second messengers involved in bitter taste and show here
for the first time that they are rapid and transient. Using a quench
-flow system we have studied bitter taste signal transduction in a
pair of mice that differ in their ability to taste the bitter
stimulus sucrose octaacetate (SOA); however, both strains taste the
bitter agent denatonium. In both strains of mice denatonium (10 mM)
induced a transient and rapid increase in levels of the second
messenger inositol 1,4,5-trisphosphate (IP3) with a maximal
production near 75-100 milliseconds after stimulation. In contrast,
SOA (100 [mu]M) brought about a similar increase in IP3 only in SOA
-taster mice. The response to SOA was potentiated in the presence of
GTP (1 [mu]M). The GTP-enhanced SOA-response supports a G-protein
mediated response for this bitter compound. The rapid kinetics,
transient nature and the specificity of the bitter taste-stimulus
induced IP3 formation are consistent with the role of IP3 as a second
messenger in the chemo-electrical transduction of bitter taste.
Received 2 November 1994; accepted in final form 14 September
1995.
APS Manuscript Number C653-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95