scholarly journals Modulation of Rat Chorda Tympani NaCl Responses and Intracellular Na+ Activity in Polarized Taste Receptor Cells by pH

2002 ◽  
Vol 120 (6) ◽  
pp. 793-815 ◽  
Author(s):  
Vijay Lyall ◽  
Rammy I. Alam ◽  
Tam-Hao T. Phan ◽  
Oneal F. Russell ◽  
Shahbaz A. Malik ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Taste Receptor ◽  
Potassium Acetate ◽  
Chorda Tympani ◽  
Receptor Cells ◽  
Intracellular Na Activity ◽  
Taste Receptor Cells ◽  
Nerve Recordings ◽  
Acid Loading ◽  
External Ph

Mixture interactions between sour and salt taste modalities were investigated in rats by direct measurement of intracellular pH (pHi) and Na+ activity ([Na+]i) in polarized fungiform taste receptor cells (TRCs) and by chorda tympani (CT) nerve recordings. Stimulating the lingual surface with NaCl solutions adjusted to pHs ranging between 2.0 and 10.3 increased the magnitude of NaCl CT responses linearly with increasing external pH (pHo). At pH 7.0, the epithelial sodium channel (ENaC) blocker, benzamil, decreased NaCl CT responses and inhibited further changes in CT responses induced by varying pHo to 2.0 or 10.3. At constant pHo, buffering NaCl solutions with potassium acetate/acetic acid (KA/AA) or HCO3−/CO2 inhibited NaCl CT responses relative to CT responses obtained with NaCl solutions buffered with HEPES. The carbonic anhydrase blockers, MK-507 and MK-417, attenuated the inhibition of NaCl CT responses in HCO3−/CO2 buffer, suggesting a regulatory role for pHi. In polarized TRCs step changes in apical pHo from 10.3 to 2.0 induced a linear decrease in pHi that remained within the physiological range (slope = 0.035; r2 = 0.98). At constant pHo, perfusing the apical membrane with Ringer's solutions buffered with KA/AA or HCO3−/CO2 decreased resting TRC pHi, and MK-507 or MK-417 attenuated the decrease in pHi in TRCs perfused with HCO3−/CO2 buffer. In parallel experiments, TRC [Na+]i decreased with (a) a decrease in apical pH, (b) exposing the apical membrane to amiloride or benzamil, (c) removal of apical Na+, and (d) acid loading the cells with NH4Cl or sodium acetate at constant pHo. Diethylpyrocarbonate and Zn2+, modification reagents for histidine residues in proteins, attenuated the CO2-induced inhibition of NaCl CT responses and the pHi-induced inhibition of apical Na+ influx in TRCs. We conclude that TRC pHi regulates Na+-influx through amiloride-sensitive apical ENaCs and hence modulates NaCl CT responses in acid/salt mixtures.

A Novel Pharmacological Probe Links the Amiloride-Insensitive NaCl, KCl, and NH4Cl Chorda Tympani Taste Responses

2001 ◽  
Vol 86 (5) ◽  
pp. 2638-2641 ◽  
Author(s):  
John A. DeSimone ◽  
Vijay Lyall ◽  
Gerard L. Heck ◽  
Tam-Hao T. Phan ◽  
Rammy I. Alam ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Apical Membrane ◽  
Cetylpyridinium Chloride ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Intracellular Acidification ◽  
Cellular Origin ◽  
Receptor Cells ◽  
Nacl Concentration

Chorda tympani taste nerve responses to NaCl can be dissected pharmacologically into amiloride-sensitive and -insensitive components. It is now established that the amiloride-sensitive, epithelial sodium channel acts as a sodium-specific ion detector in taste receptor cells (TRCs). Much less is known regarding the cellular origin of the amiloride-insensitive component, but its anion dependence indicates an important role for paracellular shunts in the determination of its magnitude. However, this has not precluded the possibility that undetected apical membrane ion pathways in TRCs may also contribute to its origin. Progress toward making such a determination has suffered from lack of a pharmacological probe for an apical amiloride-insensitive taste pathway. We present data here showing that, depending on the concentration used, cetylpyridinium chloride (CPC) can either enhance or inhibit the amiloride-insensitive response to NaCl. The CPC concentration giving maximal enhancement was 250 μM. At 2 mM, CPC inhibited the entire amiloride-insensitive part of the NaCl response. The NaCl response is, therefore, composed entirely of amiloride- and CPC-sensitive components. The magnitude of the maximally enhanced CPC-sensitive component varied with the NaCl concentration and was half-maximal at [NaCl] = 62 ± 11 (SE) mM. This was significantly less than the corresponding parameter for the amiloride-sensitive component (268 ± 71 mM). CPC had similiar effects on KCl and NH4Cl responses except that in these cases, after inhibition with 2 mM CPC, a significant CPC-insensitive response remained. CPC (2 mM) inhibited intracellular acidification of TRCs due to apically presented NH4Cl, suggesting that CPC acts on an apical membrane nonselective cation pathway.

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.

Excitation and Adaptation in the Detection of Hydrogen Ions by Taste Receptor Cells: A Role for cAMP and Ca2+

2002 ◽  
Vol 87 (1) ◽  
pp. 399-408 ◽  
Author(s):  
Vijay Lyall ◽  
Rammy I. Alam ◽  
Tam-Hao T. Phan ◽  
Duy Q. Phan ◽  
Gerard L. Heck ◽  
...  
Keyword(s):  
Voltage Clamp ◽  
Basolateral Membrane ◽  
Taste Receptor ◽  
Intracellular Camp ◽  
Receptor Cells ◽  
Zero Current ◽  
Taste Receptor Cells ◽  
Hcl Concentration ◽  
Nerve Recordings ◽  
Strong Acids

The role of intracellular cAMP and Ca2+ in the excitation and adaptation of taste responses by HCl was investigated by direct measurement of intracellular pH (pHi) in polarized taste receptor cells (TRCs) and by chorda tympani (CT) nerve recordings. Stimulating the tongue with HCl concentrations between 1 and 30 mM caused a dose-dependent increase in CT responses that were insensitive to voltage clamp of the lingual receptive field and to amiloride. At a fixed HCl concentration (20 mM) topical lingual application of 8-chlorophenylthio(CPT)-cAMP increased the magnitude of HCl-induced CT response by twofold under zero current clamp. The magnitude of the CT response increased further at −60 mV and decreased at +60 mV lingual voltage clamp but remained amiloride insensitive. In untreated polarized TRCs, apical stimulation with HCl concentrations between 1 and 30 mM HCl induced sustained decreases in TRC pHi. The magnitude of pHidecrease increased with increasing HCl concentration. Following treatment of the basolateral membrane with 8-CPT-cAMP the decrease in pHi due to apical 1 mM HCl application was significantly increased. Treatment with cAMP alone decreased resting TRC pHi and inhibited the recovery of pHi from a basolateral NH4Cl pulse by 46%. Topical lingual application of ionomycin, a Ca2+ ionophore, did not affect the initial CT response to 20 mM HCl +10 mM CaCl2, but the response declined rapidly to 50% of its initial level within 2 min. In polarized TRCs, basolateral exposure to ionomycin increased TRC pHi and activated pHi recovery from NH4Cl pulse by 388%. Apical HCl stimulation induced a transient decrease in resting TRC pHifollowed by spontaneous recovery. The data suggest that cAMP enhances the sour taste of strong acids by activating a Ca2+- and amiloride-insensitive H+ conductance and inhibiting pHi recovery in TRCs. However, an increase in [Ca2+]i stimulates pHi recovery, which, in turn, increases sensory adaptation to acids.

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
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