Salt Taste Transduction Occurs Through an Amiloride-Sensitive Sodium Transport Pathway

Heck, Gerard L.; Mierson, Sheella; DeSimone, John A.

doi:10.1126/science.6691151

Cited by 476 publications

(246 citation statements)

References 10 publications

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“…A seminal finding was published by Heck et al [38] in 1984 when they reported that Na + permeates cation channels in taste cells, specifically, amiloride-sensitive ENaCs (similar to those found in the kidney) on the anterior tongue. Passive Na + influx through ion channels, driven by the presence of Na salts in the stimulus (that is, a Na + concentration gradient favoring Na + influx), would depolarize and thereby excite taste receptor cells.…”

Section: Salty Chemosensory Transductionmentioning

confidence: 99%

Signal transduction and information processing in mammalian taste buds

Roper

2007

Pflugers Arch - Eur J Physiol

266

215

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The molecular machinery for chemosensory transduction in taste buds has received considerable attention within the last decade. Consequently, we now know a great deal about sweet, bitter, and umami taste mechanisms and are gaining ground rapidly on salty and sour transduction. Sweet, bitter, and umami tastes are transduced by G-protein-coupled receptors. Salty taste may be transduced by epithelial Na channels similar to those found in renal tissues. Sour transduction appears to be initiated by intracellular acidification acting on acidsensitive membrane proteins. Once a taste signal is generated in a taste cell, the subsequent steps involve secretion of neurotransmitters, including ATP and serotonin. It is now recognized that the cells responding to sweet, bitter, and umami taste stimuli do not possess synapses and instead secrete the neurotransmitter ATP via a novel mechanism not involving conventional vesicular exocytosis. ATP is believed to excite primary sensory afferent fibers that convey gustatory signals to the brain. In contrast, taste cells that do have synapses release serotonin in response to gustatory stimulation. The postsynaptic targets of serotonin have not yet been identified. Finally, ATP secreted from receptor cells also acts on neighboring taste cells to stimulate their release of serotonin. This suggests that there is important information processing and signal coding taking place in the mammalian taste bud after gustatory stimulation.

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Section: Salty Chemosensory Transductionmentioning

confidence: 99%

Signal transduction and information processing in mammalian taste buds

Roper

2007

Pflugers Arch - Eur J Physiol

266

215

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“…In rodents, treating the anterior tongue with amiloride, an epithelial Na + channel blocker, disrupts performance on sodium discrimination tasks (Spector et al, 1996) and inhibits chorda tympani responses to NaCl (Heck et al, 1984). Consequently, it is believed that sodium taste is transduced via the influx of Na + through epithelial sodium channels (ENaC) in the anterior tongue.…”

Section: Peripheral Gustatory Processingmentioning

confidence: 99%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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Nearly three-quarters of a century ago, Curt Richter removed the adrenal glands from rats and noted that the animal's vitality was dependent on its increased consumption of sodium chloride. In doing so, Richter revealed an innate behavioral mechanism that serves to maintain the hydromineral balance of an animal faced with sodium deficit. This experiment and others like it, led to the development of a field of research devoted to the investigation of salt appetite. The following is a discussion of how Richter's initial observations gave birth to an evolving field that incorporates multiple approaches to examine the drive to consume sodium. KeywordsSalt appetite; Angiotensin; Aldosterone; Corticosterone; Richter The Discovery of Salt AppetiteAt the time that Richter began his career at Johns Hopkins University much of the research examining ingestive behavior focused on the responses of individual organs or closely coordinated systems. Richter's pioneering work initiated a fundamental paradigm shift that moved the focus to adaptations of the organism as a whole. Specifically, he was interested in changes in behavior that compensated for perturbations in the internal environment. His approach toward investigation of such behaviors was as thorough as it was fundamental. Richter manipulated diet, interfered with the nervous system, and removed or replaced glandular secretions in attempt to understand the nutritional, neural, and endocrine signals that contribute to behavior.Richter created disturbances in the nutritional or mineral content of the internal environment with dietary deficiency. Subsequently, "self selection" experiments were performed where choices of different minerals and nutrients were presented for consumption. More often than not, animals would consume minerals and nutrients in amounts that would alleviate their experimentally-induced deficiencies. One of the most striking behaviors that Richter observed was that of rats voluntarily ingesting salt when faced with sodium deficit. Sodium chloride was removed from the rats' food and they were given access to water and 3 % NaCl solution. The intake of the NaCl solution was approximately 1% of the total diet, which remarkably, is the

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“…All solutions of glutamate agonists were titrated to pH 6.0-7.0 to avoid potential complications introduced by acid taste. Also, all solutions, including water, contained 30 pM amiloride to minimize the contribution of Na+ taste (Heck et al, 1984;Yamamoto et al, 1991;Gilbertson and Gilbertson, 1994). Half of the rats for each taste stimulus were injected intraperitoneally with 0.3 M LiCl (at 1 ml/100 gm body weight).…”

Section: Methodsmentioning

confidence: 99%

The Taste of Monosodium Glutamate: Membrane Receptors in Taste Buds

et al. 1996

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Receptor proteins for photoreception have been studied for several decades. More recently, putative receptors for olfaction have been isolated and characterized. In contrast, no receptors for taste have been identified yet by molecular cloning. This report describes experiments aimed at identifying a receptor responsible for the taste of monosodium glutamate (MSG). Using reverse transcriptase (IV)-PCR, we found that several ionotropic glutamate receptors are present in rat lingual tissues. However, these receptors also could be detected in lingual tissue devoid of taste buds. On the other hand, RT-PCR and RNase protection assays indicated that a G-protein-coupled metabotropic glutamate receptor, mGluR4, also is expressed in lingual tissues and is limited only to taste buds. In situ hybridization demonstrated that mGluR4 is detectable in 40-70% of vallate and foliate taste buds but not in surrounding nonsensory epithelium, confirming the localization of this metabotropic receptor to gustatory cells. Expression of mGluR4 in taste buds is higher in preweaning rats compared with adult rats. This may correspond to the known higher sensitivity to the taste of MSG in juvenile rodents. Finally, behavioral studies have indicated that MSG and L-2-amino-4-phosphonobutyrate (L-AP4), a ligand for mGluR4, elicit similar tastes in rats. We conclude that mGluR4 may be a chemosensory receptor responsible, in part, for the taste of MSG.

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Salt Taste Transduction Occurs Through an Amiloride-Sensitive Sodium Transport Pathway

Cited by 476 publications

References 10 publications

Signal transduction and information processing in mammalian taste buds

Signal transduction and information processing in mammalian taste buds

Richter and sodium appetite: From adrenalectomy to molecular biology

The Taste of Monosodium Glutamate: Membrane Receptors in Taste Buds

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