The molecular physiology of taste transduction

Gilbertson, Timothy A.; Damak, Sami; Margolskee, Robert F.

doi:10.1016/s0959-4388(00)00118-5

Cited by 239 publications

(150 citation statements)

References 69 publications

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“…Taste responses to bitter, sweet, and umami compounds are initiated by G-protein-coupled receptors (GPCRs) and transduced via G-protein signaling cascades (for review, see Chaudhari and Roper, 1998;Gilbertson et al, 2000;Lindemann, 2001). During the past few years, several GPCRs have been identified in taste cells and implicated in taste signal transduction Chandrashekar et al, 2000;Chaudhari et al, 2000;Max et al, 2001;Nelson et al, 2001Nelson et al, , 2002Li et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

UmamiTaste Responses Are Mediated by α-Transducin and α-Gustducin

He¹,

Yasumatsu²,

Varadarajan³

et al. 2004

J. Neurosci.

138

107

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The sense of taste comprises at least five distinct qualities: sweet, bitter, sour, salty, and umami, the taste of glutamate. For bitter, sweet, and umami compounds, taste signaling is initiated by binding of tastants to G-protein-coupled receptors in specialized epithelial cells located in the taste buds, leading to the activation of signal transduction cascades. ␣-Gustducin, a taste cell-expressed G-protein ␣ subunit closely related to the ␣-transducins, is a key mediator of sweet and bitter tastes. ␣-Gustducin knock-out (KO) mice have greatly diminished, but not entirely abolished, responses to many bitter and sweet compounds. We set out to determine whether ␣-gustducin also mediates umami taste and whether rod ␣-transducin (␣ t-rod ), which is also expressed in taste receptor cells, plays a role in any of the taste responses that remain in ␣-gustducin KO mice. Behavioral tests and taste nerve recordings of single and double KO mice lacking ␣-gustducin and/or ␣ t-rod confirmed the involvement of ␣-gustducin in bitter (quinine and denatonium) and sweet (sucrose and SC45647) taste and demonstrated the involvement of ␣-gustducin in umami [monosodium glutamate (MSG), monopotassium glutamate (MPG), and inosine monophosphate (IMP)] taste as well. We found that ␣ t-rod played no role in taste responses to the salty, bitter, and sweet compounds tested or to IMP but was involved in the umami taste of MSG and MPG. Umami detection involving ␣-gustducin and ␣ t-rod occurs in anteriorly placed taste buds, however taste cells at the back of the tongue respond to umami compounds independently of these two G-protein subunits.

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Section: Introductionmentioning

confidence: 99%

UmamiTaste Responses Are Mediated by α-Transducin and α-Gustducin

He¹,

Yasumatsu²,

Varadarajan³

et al. 2004

J. Neurosci.

138

107

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show abstract

“…ultiple signal transduction mechanisms in taste cells detect sweet, sour, bitter, salty, and umami tastes and involve both receptormediated second messenger pathways and direct interactions with ion channels (1)(2)(3). Four mechanisms have been identified for signal transduction by bitter compounds.…”

mentioning

confidence: 99%

Stimulation of Insulin Secretion by Denatonium, One of the Most Bitter-Tasting Substances Known

et al. 2003

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Denatonium, one of the most bitter-tasting substances known, stimulated insulin secretion in clonal HIT-T15 ␤-cells and rat pancreatic islets. Stimulation of release began promptly after exposure of the ␤-cells to denatonium, reached peak rates after 4 -5 min, and then declined to near basal values after 20 -30 min. In islets, no effect was observed at 2.8 mmol/l glucose, whereas a marked stimulation was observed at 8. M ultiple signal transduction mechanisms in taste cells detect sweet, sour, bitter, salty, and umami tastes and involve both receptormediated second messenger pathways and direct interactions with ion channels (1-3). Four mechanisms have been identified for signal transduction by bitter compounds. Two mechanisms result from bitter substances interacting with receptors of the T2R/TRB family and activation of gustducin (4 -10). In one, the ␣-subunit of gustducin activates cyclic nucleotide phosphodiesterase activity to decrease cyclic nucleotide monophosphate (cyclic NMP) levels and de-inhibit the activity of a cyclic NMP-inhibited cation channel leading to depolarization and increased [Ca 2ϩ ] i (11,12). In the second, the ␤␥-subunits of gustducin (probably ␤1␥13 and/or ␤3␥13) activate PLC␤2 and increase IP 3 and DAG levels (13,14). IP 3 increases [Ca 2ϩ ] i via IP 3 R3 activation (14 -16). A third mechanism involves a direct interaction and inhibition of K ϩ channels resulting in depolarization and increased [Ca 2ϩ ] i (17). The fourth known mechanism is the direct gating of nonselective cation channels and depolarization, again leading to increased [Ca 2ϩ ] i (18 -20). In all cases, increased [Ca 2ϩ ] i leads to increased neurotransmitter release and activation of the afferent gustatory nerves that transmit the bitter signal to the brain. There is evidence for the activation of multiple second messenger pathways in individual taste cells (4). There is also evidence that some bitter stimuli activate only subpopulations of bitter-sensitive taste cells (4 -6). Also, individual taste cells can respond selectively to different bitter substances (7). However, there is still much that is unknown about individual taste cell regulation.Stimulation of taste cell membranes with denatonium activates not only gustducin but also transducin (9), with which it shares high sequence homology (21). Because transducin mRNA is reported to be present in pancreatic islets at approximately one-fifth the level of that in the retina (22), we were interested to determine the effects of denatonium on insulin secretion in ␤-cells as a tool to study the potential involvement of gustducin or transducin in stimulus-secretion coupling. The experiments described here were performed on clonal HIT-T15 cells and rat pancreatic islets. RESEARCH DESIGN AND METHODSCell culture. Clonal HIT-T15 cells were cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum, 100 g/ml streptomycin, and 100 units/ml penicillin in an atmosphere of 95% air and 5% CO 2 . Cells of passage numbers 72-85 were used for the expe...

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“…These fi ndings indicate that two signal transduction pathways may be involved in the transduction of signals from denatonium: one PLC-dependent, perhaps signalling via liberation of calcium ion stores, and a PDE-dependent pathway, perhaps signalling via inhibition of cAMP. Interestingly, a similar dual signal transduction system underlying the response to denatonium is postulated by Gilbertson et al (2000) for vertebrate cells. The suggestion that more than one transduction system and one signalling pathway are involved in the perception of bitter-tastes by codling moth larvae corroborates earlier work that postulate the same for the response of larvae of Manduca sexta to bitter compounds (Glendinning & Hills, 1997;Glendinning et al, 2002).…”

Section: Effects Of Signal Transduction Modulators On Feeding Commencmentioning

confidence: 72%

“…However, there is also evidence that in some vertebrate systems, denatonium taste may be transduced via a signalling pathway independent of the phospholipase C-signalling cascade (Ruiz-Avila et al, 1995). Here, a protein α-gustducin is activated by denatonium membrane receptors, stimulates phosphodiesterase to hydrolyze cyclic adenosine monophosphate (cAMP), and consequently causes a transient decrease in cAMP level, a process that liberates calcium ions from internal calcium ion stores (Gilbertson et al, 2000;Margolskee, 2002). In mice, there are two classes of taste cells: those in which denatonium signals via a transduction pathway dependent on a G-protein, and others that respond to denatonium via a G-protein-independent pathway (Sawano et al, 2005).…”

Section: Effects Of Signal Transduction Modulators On Feeding Commencmentioning

confidence: 99%

Pharmacological analysis of the feeding response of codling moth (Cydia pomonella; Lepidoptera: Tortricidae) neonates to bitter compounds

Pszczółkowski¹

2017

Eur. J. Entomol.

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Abstract. Feeding in codling moth neonate caterpillars was inhibited by 0.67 mM and 2.24 mM concentrations of denatonium benzoate. This inhibitory effect was abolished by phospholipase C inhibitor, U-73122 and the phosphodiesterase inhibitor, Rolipram. Quinine and quinidine did not have inhibitory effects at concentrations as high as 1.64 mM and 0.43 mM, respectively. The inhibitory effect of denatonium was partially reversed in the presence of the calcium ion chelator, EGTA, at concentrations ranging from 2.5 μM to 250 μM. These results indicate that transduction of the taste of denatonium in codling moth neonates relies on signalling pathways that involve phospholipase C, phosphodiesterase and calcium ion infl ux into cells.

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The molecular physiology of taste transduction

Cited by 239 publications

References 69 publications

UmamiTaste Responses Are Mediated by α-Transducin and α-Gustducin

UmamiTaste Responses Are Mediated by α-Transducin and α-Gustducin

Stimulation of Insulin Secretion by Denatonium, One of the Most Bitter-Tasting Substances Known

Pharmacological analysis of the feeding response of codling moth (Cydia pomonella; Lepidoptera: Tortricidae) neonates to bitter compounds

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