Epithelial Na+ channel subunits in rat taste cells: Localization and regulation by aldosterone

Lin, Weihong; Finger, Thomas E.; Rossier, Bernard C.; Kinnamon, Sue C.

doi:10.1002/(sici)1096-9861(19990315)405:3<406::aid-cne10>3.0.co;2-f

Cited by 181 publications

(135 citation statements)

References 47 publications

(65 reference statements)

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“…Aldosterone elevates amiloride suppression of chorda tympani responses to NaCl (Herness, 1992) and intensifies apical immunoreactivity for subunits of the ENaC located in the taste cells on the anterior tongue (Lin et al, 1999). These studies suggest that aldosterone amplifies gustatory responses to NaCl by increasing the activity of the ENaC (Herness, 1992).…”

Section: Peripheral Gustatory Processingmentioning

confidence: 76%

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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Section: Peripheral Gustatory Processingmentioning

confidence: 76%

Richter and sodium appetite: From adrenalectomy to molecular biology

Krause

Sakai

2007

Appetite

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“…In rats, ENaC and BNC1 are expressed at the apical membrane of taste cells, where they are hypothesized to mediate salt (13,14) and sour (15) taste, respectively. However, the role of these channels in human taste is unclear.…”

Section: Discussionmentioning

confidence: 99%

“…BNC1 and all three ENaC subunits (␣, ␤, ␥) are also expressed in the tongue. On the basis of their localization in the apical membrane of taste receptor cells, DEG͞ENaC subunits may be receptors for salt taste (ENaC) (12)(13)(14) and sour taste (BNC1) (15). Consistent with these hypotheses, salt taste can be modulated in rats by the ENaC blocker amiloride or hormones that regulate ENaC activity (13,14), and BNC1 is activated at proton concentrations that elicit sour taste (15).…”

mentioning

confidence: 92%

DEG/ENaC ion channels involved in sensory transduction are modulated by cold temperature

Askwith

Benson

Welsh

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

154

102

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Several DEG͞ENaC cation channel subunits are expressed in the tongue and in cutaneous sensory neurons, where they are postulated to function as receptors for salt and sour taste and for touch. Because these tissues are exposed to large temperature variations, we examined how temperature affects DEG͞ENaC channel function. We found that cold temperature markedly increased the constitutively active Na ؉ currents generated by epithelial Na ؉ channels (ENaC). Half-maximal stimulation occurred at 25°C. Cold temperature did not induce current from other DEG͞ENaC family members (BNC1, ASIC, and DRASIC). However, when these channels were activated by acid, cold temperature potentiated the currents by slowing the rate of desensitization. Potentiation was abolished by a ''Deg'' mutation that alters channel gating. Temperature changes in the physiologic range had prominent effects on current in cells heterologously expressing acid-gated DEG͞ENaC channels, as well as in dorsal root ganglion sensory neurons. The finding that cold temperature modulates DEG͞ENaC channel function may provide a molecular explanation for the widely recognized ability of temperature to modify taste sensation and mechanosensation.T emperature is known to modulate sensations such as taste and touch. For example, personal experience informs us that temperature is key to the taste of food and wine. The interplay between temperature and sensory perception may occur by many mechanisms, including the direct action of temperature on sensory receptors.Recent studies have suggested that several members of the DEG͞ENaC family of cation channels may function as sensory receptors (for reviews see refs. 1 and 2). In Caenorhabditis elegans, the DEG͞ENaC channel subunits MEC-4 and MEC-10 are expressed in touch cell neurons, where they are thought to form part of the mechanoreceptor complex (3). In mammals, the DEG͞ENaC channel BNC1 (4) [also called MDEG (5), BNaC1 (6), and ASIC2 (2)] is expressed in lanceolate nerve endings at the site of mechanotransduction (7). Targeted disruption of the BNC1 gene in mice reduced the sensitivity of low-threshold, rapidly adapting mechanoreceptors, indicating that BNC1 is required for normal touch sensation (7). The related channel subunits ASIC (8) [also called BNaC2 (6) and ASIC1 (2)] and DRASIC (9) [also called ASIC3 (2)] are also expressed in peripheral sensory neurons; because they are activated by acidic pH, it has been proposed that they play a role in nociception (2). The mammalian epithelial Na ϩ channel (ENaC) subunits may also function in touch sensation; ␤-and ␥ENaC are expressed in Merkel cell͞neurite complexes, in lamellated corpuscles of the rat foot pad, and in lanceolate nerve endings of the vibrissal follicle (10, 11). BNC1 and all three ENaC subunits (␣, ␤, ␥) are also expressed in the tongue. On the basis of their localization in the apical membrane of taste receptor cells, DEG͞ENaC subunits may be receptors for salt taste (ENaC) (12-14) and sour taste (BNC1) (15). Consistent with these hypotheses, salt taste ...

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“…The epithelial sodium channel receptor for sodium in rodents is called ENaC (Lin et al 1999). Sodium present in the oral cavity can travel through the sodium channel formed by ENaC and trigger an action potential in the taste cell.…”

Section: Taste (Gustation)mentioning

confidence: 99%

“…Long-term mechanisms may also be mediated by peripheral mechanisms. For example, during a nutritional sodium deficiency, high levels of the renal hormone aldosterone induce the expression of the sodium channel ENaC (Lin et al 1999). This upregulation of sodium receptors increases the taste sensitivity for sodium and aids in the specific appetite for this nutrient.…”

mentioning

confidence: 99%

Unfolding the codes of short-term feed appetence in farm and companion animals. A comparative oronasal nutrient sensing biology review

Roura¹,

Humphrey²,

Tedó³

et al. 2008

Can. J. Anim. Sci.

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Roura, E., Humphrey, B., Tedo´, G. and Ipharraguerre, I. 2008. Unfolding the codes of short-term feed appetence in farm and companion animals. A comparative oronasal nutrient sensing biology review. Can. J. Anim. Sci. 88: 535Á558. The evolution of the chemical senses has resulted in a sensory apparatus for high taste and smell acuity in mammals and birds to ensure self-nourishment. Such peripheral chemosensory systems function as a code to unfold the nutritional value of feedstuffs. Food ingestion simultaneously evokes odor, taste and thermo-mechanical (somatosensing) sensations. Olfaction represents the capacity to identify feed volatiles that are predominantly derived from essential nutrients in plants.Comparative biology of olfaction shows that primates and chickens have a smaller olfactory epithelium and fewer olfactory receptor (OR) genes than non-primate mammals studied to date including farm and companion animals, such as the pig, the cow, the dog, the cat and the horse. A significant proportion of the total OR genes in mammals and birds have lost their functionality (pseudogenes) in a process that seems to reflect a decrease in the animal's reliance on the sense of smell, particularly in humans and cows. The taste system allows animals to recognize a diverse repertoire of nutrient (sugars, amino acids, salts, acids and fats) or toxic related chemical entities that provide valuable information about the quality of food. Taste senses non-volatile molecules in the oral cavity through taste receptors (TR). The TR are expressed in the sensory cells forming the taste buds of the tongue's papillae. Taste cells are linked to a network of solitary chemosensory cells diffused through many non-taste tissues involved in metabolic homeostasis. The number of functional taste receptor genes (TASR) in humans is equivalent to that in other mammals and superior to that in chickens. The TASR family 1 (TAS1R coding for umami and sweet TR) is conserved, in number and type, across the species evaluated, with the exception of the sweet receptor in chicken and feline species. The TASR family 2 (TAS2R coding for bitter TR) shows a strong adaptive capacity to dietary sources and digestive physiology across vertebrates. Pseudogenization (loss of gene functionality) in the TAS2R family seems to be a frequent strategy. The implications of oronasal nutrient sensing related to comparative animal feeding strategies and behaviors such as neophobia, feed refusal and hedonic preferences are discussed. Feed palatability and appetence might be one of the main driving forces in short-term feed consumption. Finally, practical applications relevant to animal production are outlined.Key words: Nutrient sensing, taste, olfaction, somatosensing, feed intake, farm, companion animals Roura, E., Humphrey, B., Tedo´, G. et Ipharraguerre, I. 2008. Le code de l'appe´tence a`court terme chez les animaux domestiques et de compagnie. Biologie comparative de la de´tection bucco-nasale des e´le´ments nutritifs. Can. J. Anim. Sci. 88: 535Á558. En e´voluant, ...

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Epithelial Na+ channel subunits in rat taste cells: Localization and regulation by aldosterone

Cited by 181 publications

References 47 publications

Richter and sodium appetite: From adrenalectomy to molecular biology

Richter and sodium appetite: From adrenalectomy to molecular biology

DEG/ENaC ion channels involved in sensory transduction are modulated by cold temperature

Unfolding the codes of short-term feed appetence in farm and companion animals. A comparative oronasal nutrient sensing biology review

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