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PubMed2002

A quantitative study of fungiform papillae and taste pore density in adults and children.

Male children (8-9 years) are reported to have a higher sensitivity than male adults to the sweet tastant sucrose when small regions of the anterior tongue are stimulated. The present study investigated the hypothesis that the higher sensitivity was due to a greater density of fungiform papillae and taste pores (buds), since it has been reported in adults that increased densities of these two structures correlates with increased taste suprathreshold sensitivity [Physiol. Behav. 47 (1990) 1213]. Quantitative measures of the number and size of papillae and pores in two areas of the tongue that had been shown to have a higher sensitivity for sucrose were achieved in 20 male children 8-9 years of age and 20 adults 18-30 years of age, using videomicroscopy and NIH Image software. Customized templates and a red food dye were used to define the equivalent tongue locations across the 40 subjects and taste pores were stained with methylene blue. Children were found to have substantially smaller papillae than adults but significantly higher papilla densities in both areas. Similar numbers of taste pores per papilla were found for both groups, resulting in children having much higher taste pore densities in each area than adults. Other differences included smaller taste pore diameters in children compared to adults, and the papillae tended to be rounder in children. Overall, the results support the hypothesis that the higher densities of fungiform papillae and taste pores in children underlie their greater sensitivity for sucrose in the two areas. In addition, the anatomical differences between adults and children indicate the sense of taste is in a state of development during mid-childhood.

Adolescent↗
PubMed2004

Receptors for bitter, sweet and umami taste couple to inhibitory G protein signaling pathways.

Taste receptors are thought to couple to the G protein Galpha-gustducin to initiate signal transduction cascades leading to taste perception. To further characterize the G protein-coupling selectivity of these receptors, we expressed them in HEK293 cells and monitored the modulation of different signaling pathways upon stimulation. We found that the bitter compound cycloheximide induces phosphorylation of extracellular signal-regulated kinases1 and 2 (ERK 1/2) and inhibits cAMP accumulation in HEK293 cells expressing the mouse bitter T2R(5) receptor. These effects are totally abolished upon treatment with pertussis toxin. On the other hand, sweeteners and monosodium glutamate induce phosphorylation of ERK1/2 and inhibit cAMP accumulation in HEK293 cells expressing the human sweet T1R(2)/T1R(3) receptor and the human umami T1R(1)/T1R(3) receptor, respectively. The effects of these taste modalities are also prevented by treatment with pertussis toxin. Collectively, our results show that taste receptors can functionally couple to Galpha(i/o) proteins to transmit intracellular signals.

Adenylyl Cyclase Inhibitors↗
PubMed2000

T2Rs function as bitter taste receptors.

Bitter taste perception provides animals with critical protection against ingestion of poisonous compounds. In the accompanying paper, we report the characterization of a large family of putative mammalian taste receptors (T2Rs). Here we use a heterologous expression system to show that specific T2Rs function as bitter taste receptors. A mouse T2R (mT2R-5) responds to the bitter tastant cycloheximide, and a human and a mouse receptor (hT2R-4 and mT2R-8) responded to denatonium and 6-n-propyl-2-thiouracil. Mice strains deficient in their ability to detect cycloheximide have amino acid substitutions in the mT2R-5 gene; these changes render the receptor significantly less responsive to cycloheximide. We also expressed mT2R-5 in insect cells and demonstrate specific tastant-dependent activation of gustducin, a G protein implicated in bitter signaling. Since a single taste receptor cell expresses a large repertoire of T2Rs, these findings provide a plausible explanation for the uniform bitter taste that is evoked by many structurally unrelated toxic compounds.

Afferent Pathways↗