Receptor that leaves a sour taste in the mouth

Ugawa, Shinya; Minami, Yoichi; Guo, Wei; Saishin, Yoshitsugu; Takatsuji, Koichi; Yamamoto, Takashi; Tohyama, Masaya; Shimada, Shoichi

doi:10.1038/26882

Cited by 158 publications

(101 citation statements)

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“…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: 54%

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

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Benson

Welsh

et al. 2001

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

155

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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mentioning

confidence: 54%

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.

155

102

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“…MDEG cDNA was cloned from a Sprague-Dawley rat brain cDNA library according to a previous report 9 and subcloned into pBluescript-SK(Ϫ) (Stratagene, La Jolla, Calif), referred to as pBlueG430. The HindIII-ApaI-digested fragment containing the full-length coding region of MDEG cDNA was subcloned into the pCDNA3 vector (Invitrogen, Carlsbad, Calif), referred to as CMVpCDNA3 MDEG-G430.…”

Section: Preparation Of Mutated Mdegmentioning

confidence: 99%

A novel strategy for cancer therapy by mutated mammalian degenerin gene transfer

et al. 2000

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Mammalian degenerin (MDEG) is a member of the amiloride-sensitive sodium ion channel family, and its site-directed active mutant (MDEG-G430F) induces massive Na ϩ influx into cells, leading to cell ballooning and cell bursting. We attempted a novel therapeutic approach for gastric cancers by transferring MDEG-G430F into cancer cells using tumor-specific promoters. In carcinoembryonic antigen (CEA)-producing gastric cancer cells, the level of cell death observed when MDEG-G430F was used with a CEA promoter was similar to that observed when using a potent nonspecific promoter such as the cytomegalovirus promoter. In an in vivo study, fusogenic liposome complexes containing MDEG-G430F driven by the CEA promoter were injected intraperitoneally into CEA-producing gastric cancer cells in a mouse peritoneal dissemination model. Although all 15 of the control mice were dead by 50 days postinoculation, 13 of the 15 mice treated with MDEG-G430F survived. These results indicate that transferring MDEG-G430F into cancer tissues using tumor-specific promoters can achieve striking and selective cancer cell death irrespective of the transcriptional efficiency of the promoters used in vivo, and suggest that this approach is a promising new strategy for cancer gene therapy.

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“…Previous studies revealed that ASICs are involved in a wide range of neuronal functions such as synaptic plasticity (Wemmie et al 2003), mechanosensation (Price et al 2000;, nociception linked to local tissue acidosis, sour-taste reception (Ugawa et al 1998), and the modulation of retinal and cochlear functions (Ettaiche et al 2004). It is also known that ASICs respond to an extracellular pH lower than 7.0.…”

Section: Introductionmentioning

confidence: 99%

The acid-sensing ion channel 2 (ASIC2) of ciliated cells in the developing rat nasal septum

Kikuchi

Ninomiya

Kawamata

et al. 2010

Archives of Histology and Cytology

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Receptor that leaves a sour taste in the mouth

Cited by 158 publications

References 0 publications

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

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

A novel strategy for cancer therapy by mutated mammalian degenerin gene transfer

The acid-sensing ion channel 2 (ASIC2) of ciliated cells in the developing rat nasal septum

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