Bitter taste transduced by PLC-beta(2)-dependent rise in IP(3) and alpha-gustducin-dependent fall in cyclic nucleotides |
| |
Authors: | Yan W Sunavala G Rosenzweig S Dasso M Brand J G Spielman A I |
| |
Affiliation: | Department of Basic Science and Craniofacial Biology, Division of Biological Science, Medicine, and Surgery, New York University College of Dentistry, 345 E. 24th St., New York, NY 10010, USA. |
| |
Abstract: | Current evidence points to the existence of multiple processesfor bitter taste transduction. Previous work demonstrated involvement of the polyphosphoinositide system and an -gustducin(G gust)-mediated stimulation of phosphodiesterase inbitter taste transduction. Additionally, a taste-enriched G protein -subunit, G 13, colocalizes with G gustand mediates the denatonium-stimulated production of inositol1,4,5-trisphosphate (IP3). Using quench-flow techniques, weshow here that the bitter stimuli, denatonium and strychnine, inducerapid (50-100 ms) and transient reductions in cAMP and cGMP andincreases in IP3 in murine taste tissue. This decrease ofcyclic nucleotides is inhibited by G gust antibodies,whereas the increase in IP3 is not affected by antibodiesto G gust. IP3 production is inhibited byantibodies specific to phospholipase C- 2(PLC- 2), a PLC isoform known to be activated byG![beta](http://ajpcell.physiology.org/math/12pt/normal/beta.gif) -subunits. Antibodies to PLC- 3 or toPLC- 4 were without effect. These data suggest atransduction mechanism for bitter taste involving the rapid andtransient metabolism of dual second messenger systems, both mediatedthrough a taste cell G protein, likely composed ofG gust/ / 13, with both systems beingsimultaneously activated in the same bitter-sensitive taste receptor cell. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
| 点击此处可从《American journal of physiology. Cell physiology》浏览原始摘要信息 |
|
点击此处可从《American journal of physiology. Cell physiology》下载全文 |
|