scholarly journals Role for epithelial Na+channels and putative Na+/H+ exchangers in salt taste transduction in rats

1997 ◽  
Vol 273 (6) ◽  
pp. R1923-R1931 ◽  
Author(s):  
Robert F. Lundy ◽  
David W. Pittman ◽  
Robert J. Contreras
Keyword(s):  
Salt Concentration ◽  
Taste Receptor ◽  
Drug Dose ◽  
Chorda Tympani Nerve ◽  
Sprague Dawley ◽  
Salt Taste ◽  
Receptor Cells ◽  
Taste Transduction ◽  
Taste Receptor Cells ◽  
Dimethyl Amiloride

The effects of the epithelial Na+channel antagonists amiloride and benzamil and the Na+/H+exchange antagonist 5-( N, N-dimethyl)-amiloride (DMA)-Cl on the integrated responses of the chorda tympani nerve to 30, 75, 150, 300, and 500 mM concentrations of NaCl, KCl, and NH4Cl were assessed in male Sprague-Dawley rats. Based on evidence from other systems, 1 and 25 μM amiloride and benzamil were chosen to selectively inhibit epithelial Na+ channels and 1 μM DMA was chosen to selectively inhibit Na+/H+exchange. When added to stimulating salt solutions, amiloride, benzamil, and DMA were each effective in inhibiting responses to all three salts. The degree of inhibition varied with drug, salt, and salt concentration, but not drug dose. Amiloride suppressed NaCl responses to a greater degree than KCl and NH4Cl responses, whereas DMA suppressed NH4Cl responses to a greater degree than NaCl and KCl responses. In all but one case (25 μM amiloride added to KCl), drug suppression of taste nerve responses decreased with an increase in salt concentration. The present results suggest that 1) epithelial Na+ channels in rat taste receptor cells may play a role in KCl and NH4Cl taste transduction; 2) a Na+/H+exchange protein may be present in taste receptor cells, representing a putative component, in addition to epithelial Na+ channels, in salt taste transduction; and 3) salt taste detection and transduction may depend on the utilization of a combination of common and distinct transcellular pathways.

scholarly journals Insulin activates epithelial sodium channel (ENaC) via phosphoinositide 3-kinase in mammalian taste receptor cells

2011 ◽  
Vol 300 (4) ◽  
pp. C860-C871 ◽  
Author(s):  
Arian F. Baquero ◽  
Timothy A. Gilbertson
Keyword(s):  
Sodium Channel ◽  
Taste Receptor ◽  
Epithelial Sodium Channel ◽  
Endocrine Regulation ◽  
Salt Taste ◽  
Receptor Cells ◽  
Taste Receptor Cells ◽  
Phosphoinositide 3 Kinase ◽  
20 Nm ◽  
Epithelial Sodium Channel Enac

Diabetes is a profound disease that results in a severe lack of regulation of systemic salt and water balance. From our earlier work on the endocrine regulation of salt taste at the level of the epithelial sodium channel (ENaC), we have begun to investigate the ability of insulin to alter ENaC function with patch-clamp recording on isolated mouse taste receptor cells (TRCs). In fungiform and vallate TRCs that exhibit functional ENaC currents (e.g., amiloride-sensitive Na+ influx), insulin (5–20 nM) caused a significant increase in Na+ influx at −80 mV (EC50 = 7.53 nM). The insulin-enhanced currents were inhibited by amiloride (30 μM). Similarly, in ratiometric Na+ imaging using SBFI, insulin treatment (20 nM) enhanced Na+ movement in TRCs, consistent with its action in electrophysiological assays. The ability of insulin to regulate ENaC function is dependent on the enzyme phosphoinositide 3-kinase since treatment with the inhibitor LY294002 (10 μM) abolished insulin-induced changes in ENaC. To test the role of insulin in the regulation of salt taste, we have characterized behavioral responses to NaCl using a mouse model of acute hyperinsulinemia. Insulin-treated mice show significant avoidance of NaCl at lower concentrations than the control group. Interestingly, these differences between groups were abolished when amiloride (100 μM) was added into NaCl solutions, suggesting that insulin was regulating ENaC. Our results are consistent with a role for insulin in maintaining functional expression of ENaC in mouse TRCs.

Amiloride Blocks Acid Responses in NaCl-Best Gustatory Neurons of the Hamster Solitary Nucleus

1998 ◽  
Vol 80 (3) ◽  
pp. 1362-1372 ◽  
Author(s):  
John D. Boughter ◽  
David V. Smith
Keyword(s):  
Citric Acid ◽  
Taste Receptor ◽  
Nerve Fibers ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Receptor Cells ◽  
Biophysical Studies ◽  
Taste Receptor Cells ◽  
To Receive ◽  
Gustatory Neurons

Boughter, John D., Jr. and David V. Smith. Amiloride blocks acid responses in NaCl-best gustatory neurons of the hamster solitary nucleus. J. Neurophysiol. 80: 1362–1372, 1998. Biophysical studies of isolated taste receptor cells show that one mechanism of Na+ salt transduction involves the inward movement of Na+ through amiloride-blockable ion channels on the apical receptor cell membrane, which leads to a direct depolarization. Hamster taste receptor cells with amiloride-blockable Na+ responses also show an amiloride-sensitive H+ current. Thus one mechanism for the transduction of acid taste involves the amiloride-sensitive channel. We investigated the effects of amiloride on responses to acids in neurons of the nucleus of the solitary tract (NST) of the hamster. The responses of 47 NST neurons were recorded extracellularly while the anterior tongue was stimulated with solutions representing the four taste qualities (NaCl, sucrose, HCl, quinine), which were used to characterize each cell on the basis of its best stimulus. The effects of amiloride on responses to 10 mM HCl, 10 mM citric acid, 100 mM NaCl, and 100 mM sucrose were then investigated. Stimuli were presented alone for 30 s (control trials) and also presented for 10 s, followed by a mixture of the stimulus with 10 μM amiloride for 10 s, followed by the stimulus alone again for 10 s (amiloride trials). The effects of amiloride were assessed by comparing the responses of cells with the stimulus + amiloride with that of the stimulus alone. In neurons classified as NaCl-best, amiloride reversibly blocked responses to NaCl, HCl, and citric acid. In HCl-best neurons, amiloride had no effect on responses to any of these stimuli. In sucrose-best neurons, amiloride blocked the response to NaCl but not to sucrose or to either acid. These results support the hypothesis that acids are transduced by at least two different receptor mechanisms in the hamster, amiloride sensitive and amiloride insensitive. At the NST, these inputs are tightly maintained in two separate populations of neurons. Sucrose-best neurons, which show amiloride effects on NaCl but not acids, appear to receive converging inputs from both amiloride-sensitive (N-best) and amiloride-insensitive (H-best) chorda tympani nerve fibers.

Acid-induced responses in hamster chorda tympani and intracellular pH tracking by taste receptor cells

1998 ◽  
Vol 275 (1) ◽  
pp. C227-C238 ◽  
Author(s):  
Robert E. Stewart ◽  
Vijay Lyall ◽  
George M. Feldman ◽  
Gerard L. Heck ◽  
John A. DeSimone
Keyword(s):  
Voltage Clamp ◽  
Intracellular Ph ◽  
Imaging Techniques ◽  
Taste Receptor ◽  
Channel Blockers ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Linear Change ◽  
Receptor Cells ◽  
Taste Receptor Cells

HCl- and NaCl-induced hamster chorda tympani nerve responses were recorded during voltage clamp of the lingual receptive field. Voltage perturbations did not influence responses to HCl. In contrast, responses to NaCl were decreased by submucosal-positive and increased by submucosal-negative voltage clamp. Responses to HCl were insensitive to the Na+ channel blockers, amiloride and benzamil, and to methylisobutylamiloride (MIA), an Na+/H+exchange blocker. Responses to NaCl were unaffected by MIA but were suppressed by benzamil. Microfluorometric and imaging techniques were used to monitor the relationship between external pH (pHo) and the intracellular pH (pHi) of fungiform papilla taste receptor cells (TRCs) following 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein loading. TRC pHi responded rapidly and monotonically to changes in pHo. This response was unaffected by Na+ removal or the presence of amiloride, benzamil, or MIA. The neural records and the data from isolated TRCs suggest that the principal transduction pathway for acid taste in hamster is similar to that in rat. This may involve the monitoring of changes in TRC pHimediated through amiloride-insensitive H+ transport across TRC membranes. This is an example of cell monitoring of environmental pH through pH tracking, i.e., a linear change in pHi in response to a change in pHo, as has been proposed for carotid bodies. In taste, the H+transport sites may be concentrated on the basolateral membranes of TRCs and, therefore, are responsive to an attenuated H+ concentration from diffusion of acids across the tight junctions.

Time course of saline-induced recovery of the gustatory system in sodium-restricted rats

1996 ◽  
Vol 270 (4) ◽  
pp. R704-R712 ◽  
Author(s):  
R. E. Stewart ◽  
D. L. Hill
Keyword(s):  
Time Course ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Gustatory System ◽  
Chorda Tympani Nerve ◽  
Pregnant Rats ◽  
Receptor Cells ◽  
Saline Ingestion ◽  
Delayed Recovery ◽  
Taste Receptor Cells

Placing pregnant rats on a Na(+)-restricted diet (0.03% NaCl) results in greatly reduced chorda tympani nerve responses to Na+ stimuli in the offspring. Normal responses can be permanently restored by providing offspring one-time access to saline. We tested whether saline-induced recovery occurs in taste receptor cells present at the time of saline intake. Chorda tympani responses were recorded 2 h, 6 h, 24 h, 10 days, and 20 days after saline ingestion. Chorda tympani Na+ responses from Na(+)-restricted rats at 2 h, 6 h, 24 h, and 10 days after saline intake were comparable to responses from control Na(+)-restricted rats. Twenty days after saline consumption, responses to Na+ were significantly elevated compared with control Na(+)-restricted rats. The results indicate that extant taste receptor cells are not substantially influenced by the saline ingestion. Instead, the delayed recovery suggests that taste receptor stem cells exclusively are influenced by saline intake.

Taste Transductions in Taste Receptor Cells: Basic Tastes and Moreover

2014 ◽  
Vol 20 (16) ◽  
pp. 2684-2692 ◽  
Author(s):  
Shusuke Iwata ◽  
Ryusuke Yoshida ◽  
Yuzo Ninomiya
Keyword(s):  
Taste Receptor ◽  
Receptor Cells ◽  
Taste Receptor Cells

scholarly journals Regulation of the Putative TRPV1t Salt Taste Receptor by Phosphatidylinositol 4, 5-Bisphosphate

2010 ◽  
Vol 103 (3) ◽  
pp. 1337-1349 ◽  
Author(s):  
Vijay Lyall ◽  
Tam-Hao T. Phan ◽  
ZuoJun Ren ◽  
Shobha Mummalaneni ◽  
Pamela Melone ◽  
...  
Keyword(s):  
Monosodium Glutamate ◽  
Taste Receptor ◽  
Receptor Protein ◽  
Chorda Tympani ◽  
Sprague Dawley ◽  
Salt Taste ◽  
Sprague Dawley Rats ◽  
Enhanced Ct ◽  
Biphasic Effect ◽  
Phosphatidylinositol 4

Regulation of the putative amiloride and benzamil (Bz)-insensitive TRPV1t salt taste receptor by phosphatidylinositol 4,5-bisphosphate (PIP2) was studied by monitoring chorda tympani (CT) taste nerve responses to 0.1 M NaCl solutions containing Bz (5 × 10−6 M; a specific ENaC blocker) and resiniferatoxin (RTX; 0–10 × 10−6 M; a specific TRPV1 agonist) in Sprague-Dawley rats and in wildtype (WT) and TRPV1 knockout (KO) mice. In rats and WT mice, RTX elicited a biphasic effect on the NaCl + Bz CT response, increasing the CT response between 0.25 × 10−6 and 1 × 10−6 M. At concentrations >1 × 10−6 M, RTX inhibited the CT response. An increase in PIP2 by topical lingual application of U73122 (a phospholipase C blocker) or diC8-PIP2 (a short chain synthetic PIP2) inhibited the control NaCl + Bz CT response and decreased its sensitivity to RTX. A decrease in PIP2 by topical lingual application of phenylarsine oxide (a phosphoinositide 4 kinase blocker) enhanced the control NaCl + Bz CT response, increased its sensitivity to RTX stimulation, and inhibited the desensitization of the CT response at RTX concentrations >1 × 10−6 M. The ENaC-dependent NaCl CT responses were not altered by changes in PIP2. An increase in PIP2 enhanced CT responses to sweet (0.3 M sucrose) and bitter (0.01 M quinine) stimuli. RTX produced the same increase in the Bz-insensitive Na+response when present in salt solutions containing 0.1 M NaCl + Bz, 0.1 M monosodium glutamate + Bz, 0.1 M NaCl + Bz + 0.005 M SC45647, or 0.1 M NaCl + Bz + 0.01 M quinine. No effect of RTX was observed on CT responses in WT mice and rats in the presence of the TRPV1 blocker N-(3-methoxyphenyl)-4-chlorocinnamide (1 × 10−6 M) or in TRPV1 KO mice. We conclude that PIP2 is a common intracellular effector for sweet, bitter, umami, and TRPV1t-dependent salt taste, although in the last case, PIP2 seems to directly regulate the taste receptor protein itself, i.e., the TRPV1 ion channel or its taste receptor variant, TRPV1t.

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