By studying how taste-receptor mutations impact fruit fly behavior, researchers have identified a taste receptor responsible for the detection of caffeine, a bitter compound known to activate certain taste-receptor neurons, as well as impact various aspects of physiology. The findings are reported by Craig Montell and colleagues at Johns Hopkins University, and appear in the September 19th issue of Current Biology, published by Cell Press.
Many proteins have been identified in mammals and in the genetic model organism Drosophila that belong to a large family of taste receptors, but relatively few of these receptors have been shown to be responsible for the detection of a specific taste compound, or "tastant." One class of tastants for which receptors have not yet been identified is methylxanthines, which include caffeine and related compounds in tea (theophylline) and cocoa (theobromine).
In the new work reported by Montell and colleagues, researchers showed that a specific taste receptor, known as Gr66a, is responsible for the perception of caffeine's bitter taste by fruit flies. The researchers showed that when the gene encoding the Gr66a receptor was disrupted, the mutant flies failed to react normally to the presentation of caffeine, which is a bitter compound that is aversive to flies. Flies with an intact Gr66a receptor gene strongly prefer to consume sucrose (sugar) when given a choice between sucrose and a mixture of sucrose and bitter compounds, but the researchers showed that flies bearing a mutation that disrupted Gr66a failed to show this strong propensity when the bitter mixture contained caffeine. The researchers also showed that activation of the gustatory-receptor neurons that express the Gr66a receptor was impaired in the mutants: Although these gustatory neurons were activated normally by a range of different tastants, they failed to be activated by caffeine, or by the related methylxanthine, theophylline. Another methylxanthine, theobromine, did elicit activation of the neurons, indicating that the Gr66a receptor exhibits some specificity in relaying the detection of different methylxanthine compounds to the nervous system. This observation also solidified the evidence that caffeine detection is functioning through a taste receptor, rather than a nonreceptor signaling route known to be affected by both caffeine and theobromine.
Though the route by which caffeine activates mammalian taste-receptor cells is not known, the new findings suggest that taste receptors may mediate caffeine detection in mammals.
The researchers include Seok Jun Moon, Michael Köttgen, Yuchen Jiao, and Craig Montell of Johns Hopkins University School of Medicine in Baltimore, Maryland; Hong Xu of Johns Hopkins University School of Medicine in Baltimore, Maryland and University of California, San Francisco in San Francisco, California. This work was supported by grants to M.K. from the Polycystic Kidney Disease Foundation and to C.M. from the NICDC (DC007864).
Moon et al.: "A Taste Receptor Required for the Caffeine Response In Vivo." Publishing in Current Biology 16, 1812–1817, September 19, 2006. DOI 10.1016/j.cub.2006.07.024. www.current-biology.com
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