scholarly journals Intracellular pH Modulates Taste Receptor Cell Volume and the Phasic Part of the Chorda Tympani Response to Acids

2005 ◽  
Vol 127 (1) ◽  
pp. 15-34 ◽  
Author(s):  
Vijay Lyall ◽  
Hampton Pasley ◽  
Tam-Hao T. Phan ◽  
Shobha Mummalaneni ◽  
Gerard L. Heck ◽  
...  
Keyword(s):  
Cell Volume ◽  
Intracellular Ph ◽  
Cytochalasin B ◽  
Taste Receptor ◽  
Flufenamic Acid ◽  
Chorda Tympani ◽  
Phasic Response ◽  
Rhodamine Phalloidin ◽  
Cation Conductance ◽  
Nerve Recordings

The relationship between cell volume and the neural response to acidic stimuli was investigated by simultaneous measurements of intracellular pH (pHi) and cell volume in polarized fungiform taste receptor cells (TRCs) using 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF) in vitro and by rat chorda tympani (CT) nerve recordings in vivo. CT responses to HCl and CO2 were recorded in the presence of 1 M mannitol and specific probes for filamentous (F) actin (phalloidin) and monomeric (G) actin (cytochalasin B) under lingual voltage clamp. Acidic stimuli reversibly decrease TRC pHi and cell volume. In isolated TRCs F-actin and G-actin were labeled with rhodamine phalloidin and bovine pancreatic deoxyribonuclease-1 conjugated with Alexa Fluor 488, respectively. A decrease in pHi shifted the equilibrium from F-actin to G-actin. Treatment with phalloidin or cytochalasin B attenuated the magnitude of the pHi-induced decrease in TRC volume. The phasic part of the CT response to HCl or CO2 was significantly decreased by preshrinking TRCs with hypertonic mannitol and lingual application of 1.2 mM phalloidin or 20 μM cytochalasin B with no effect on the tonic part of the CT response. In TRCs first treated with cytochalasin B, the decrease in the magnitude of the phasic response to acidic stimuli was reversed by phalloidin treatment. The pHi-induced decrease in TRC volume induced a flufenamic acid–sensitive nonselective basolateral cation conductance. Channel activity was enhanced at positive lingual clamp voltages. Lingual application of flufenamic acid decreased the magnitude of the phasic part of the CT response to HCl and CO2. Flufenamic acid and hypertonic mannitol were additive in inhibiting the phasic response. We conclude that a decrease in pHi induces TRC shrinkage through its effect on the actin cytoskeleton and activates a flufenamic acid–sensitive basolateral cation conductance that is involved in eliciting the phasic part of the CT response to acidic stimuli.

Effects of osmolarity on taste receptor cell size and function

1999 ◽  
Vol 277 (4) ◽  
pp. C800-C813 ◽  
Author(s):  
Vijay Lyall ◽  
Gerard L. Heck ◽  
John A. DeSimone ◽  
George M. Feldman
Keyword(s):  
Cell Volume ◽  
Receptor Cell ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Taste Receptor Cell ◽  
Salt Taste ◽  
Receptor Cells ◽  
Enhanced Ct ◽  
And Function ◽  
Osmotic Effects

Osmotic effects on salt taste were studied by recording from the rat chorda tympani (CT) nerve and by measuring changes in cell volume of isolated rat fungiform taste receptor cells (TRCs). Mannitol, cellobiose, urea, or DMSO did not induce CT responses. However, the steady-state CT responses to 150 mM NaCl were significantly increased when the stimulus solutions also contained 300 mM mannitol or cellobiose, but not 600 mM urea or DMSO. The enhanced CT responses to NaCl were reversed when the saccharides were removed and were completely blocked by addition of 100 μM amiloride to the stimulus solution. Exposure of TRCs to hyperosmotic solutions of mannitol or cellobiose induced a rapid and sustained decrease in cell volume that was completely reversible, whereas exposure to hypertonic urea or DMSO did not induce sustained reductions in cell volume. These data suggest that the osmolyte-induced increase in the CT response to NaCl involves a sustained decrease in TRC volume and the activation of amiloride-sensitive apical Na+ channels.

scholarly journals Ethanol Modulates the VR-1 Variant Amiloride-insensitive Salt Taste Receptor. II. Effect on Chorda Tympani Salt Responses

2005 ◽  
Vol 125 (6) ◽  
pp. 587-600 ◽  
Author(s):  
Vijay Lyall ◽  
Gerard L. Heck ◽  
Tam-Hao T. Phan ◽  
Shobha Mummalaneni ◽  
Shahbaz A. Malik ◽  
...  
Keyword(s):  
Elevated Temperature ◽  
Direct Action ◽  
Taste Receptor ◽  
Na Channel ◽  
Chorda Tympani ◽  
Sprague Dawley ◽  
Mineral Salts ◽  
Tonic Component ◽  
Salt Taste ◽  
Nerve Recordings

The effect of ethanol on the amiloride- and benzamil (Bz)-insensitive salt taste receptor was investigated by direct measurement of intracellular Na+ activity ([Na+]i) using fluorescence imaging in polarized fungiform taste receptor cells (TRCs) and by chorda tympani (CT) taste nerve recordings. CT responses to KCl and NaCl were recorded in Sprague-Dawley rats, and in wild-type (WT) and vanilloid receptor-1 (VR-1) knockout mice (KO). CT responses were monitored in the presence of Bz, a specific blocker of the epithelial Na+ channel (ENaC). CT responses were also recorded in the presence of agonists (resiniferatoxin and elevated temperature) and antagonists (capsazepine and SB-366791) of VR-1 that similarly modulate the Bz-insensitive VR-1 variant salt taste receptor. In the absence of mineral salts, ethanol induced a transient decrease in TRC volume and elicited only transient phasic CT responses. In the presence of mineral salts, ethanol increased the apical cation flux in TRCs without a change in volume, increased transepithelial electrical resistance across the tongue, and elicited CT responses that were similar to salt responses, consisting of both a phasic component and a sustained tonic component. At concentrations <50%, ethanol enhanced responses to KCl and NaCl, while at ethanol concentrations >50%, those CT responses were inhibited. Resiniferatoxin and elevated temperature increased the sensitivity of the CT response to ethanol in salt-containing media, and SB-366791 inhibited the effect of ethanol, resiniferatoxin, and elevated temperature on the CT responses to mineral salts. VR-1 KO mice demonstrated no Bz-insensitive CT response to NaCl and no sensitivity to ethanol. We conclude that ethanol increases salt taste sensitivity by its direct action on the Bz-insensitive VR-1 variant salt taste receptor.

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.

scholarly journals T1R3 taste receptor is critical for sucrose but not Polycose taste

2009 ◽  
Vol 296 (4) ◽  
pp. R866-R876 ◽  
Author(s):  
Steven Zukerman ◽  
John I. Glendinning ◽  
Robert F. Margolskee ◽  
Anthony Sclafani
Keyword(s):  
Critical Role ◽  
Taste Receptor ◽  
Sweet Taste ◽  
Sucrose Preference ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Sweet Taste Receptor ◽  
Sucrose Solutions ◽  
Nerve Recordings

In addition to their well-known preference for sugars, mice and rats avidly consume starch-derived glucose polymers (e.g., Polycose). T1R3 is a component of the mammalian sweet taste receptor that mediates the preference for sugars and artificial sweeteners in mammals. We examined the role of the T1R3 receptor in the ingestive response of mice to Polycose and sucrose. In 60-s two-bottle tests, knockout (KO) mice preferred Polycose solutions (4–32%) to water, although their overall preference was lower than WT mice (82% vs. 94%). KO mice also preferred Polycose (0.5–32%) in 24-h two-bottle tests, although less so than WT mice at dilute concentrations (0.5–4%). In contrast, KO mice failed to prefer sucrose to water in 60-s tests. In 24-h tests, KO mice were indifferent to 0.5–8% sucrose, but preferred 16–32% sucrose; this latter result may reflect the post-oral effects of sucrose. Overall sucrose preference and intake were substantially less in KO mice than WT mice. However, when retested with 0.5–32% sucrose solutions, the KO mice preferred all sucrose concentrations, although they drank less sugar than WT mice. The experience-induced sucrose preference is attributed to a post-oral conditioned preference for the T1R3-independent orosensory features of the sugar solutions (odor, texture, T1R2-mediated taste). Chorda tympani nerve recordings revealed virtually no response to sucrose in KO mice, but a near-normal response to Polycose. These results indicate that the T1R3 receptor plays a critical role in the taste-mediated response to sucrose but not Polycose.

scholarly journals Changes in taste receptor cell [Ca2+]i modulate chorda tympani responses to salty and sour taste stimuli

2012 ◽  
Vol 108 (12) ◽  
pp. 3206-3220 ◽  
Author(s):  
John A. DeSimone ◽  
ZuoJun Ren ◽  
Tam-Hao T. Phan ◽  
Gerard L. Heck ◽  
Shobha Mummalaneni ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Receptor Cell ◽  
Imaging Techniques ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Taste Receptor Cell ◽  
Atpase Inhibitor ◽  
Acetoxymethyl Ester ◽  
Phasic Response ◽  
Sour Taste

The relationship between taste receptor cell (TRC) Ca2+ concentration ([Ca2+]i) and rat chorda tympani (CT) nerve responses to salty [NaCl and NaCl+benzamil (Bz)] and sour (HCl, CO2, and acetic acid) taste stimuli was investigated before and after lingual application of ionomycin+Ca2+, 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM), U73122 (phospholipase C blocker), and thapsigargin (Ca2+-ATPase inhibitor) under open-circuit or lingual voltage-clamp conditions. An increase in TRC [Ca2+]i attenuated the tonic Bz-sensitive NaCl CT response and the apical membrane Na+ conductance. A decrease in TRC [Ca2+]i enhanced the tonic Bz-sensitive and Bz-insensitive NaCl CT responses and apical membrane Na+ conductance but did not affect CT responses to KCl or NH4Cl. An increase in TRC [Ca2+]i did not alter the phasic response but attenuated the tonic CT response to acidic stimuli. A decrease in [Ca2+]i did not alter the phasic response but attenuated the tonic CT response to acidic stimuli. In a subset of TRCs, a positive relationship between [H+]i and [Ca2+]i was obtained using in vitro imaging techniques. U73122 inhibited the tonic CT responses to NaCl, and thapsigargin inhibited the tonic CT responses to salty and sour stimuli. The results suggest that salty and sour taste qualities are transduced by [Ca2+]i-dependent and [Ca2+]i-independent mechanisms. Changes in TRC [Ca2+]i in a BAPTA-sensitive cytosolic compartment regulate ion channels and cotransporters involved in the salty and sour taste transduction mechanisms and in neural adaptation. Changes in TRC [Ca2+]i in a separate subcompartment, sensitive to inositol trisphosphate and thapsigargin but inaccessible to BAPTA, are associated with neurotransmitter release.

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.

scholarly journals Cell non-autonomous requirement of p75 in the development of geniculate oral sensory neurons

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Tang ◽  
Christopher R. Donnelly ◽  
Amol A. Shah ◽  
Robert M. Bradley ◽  
Charlotte M. Mistretta ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Significant Loss ◽  
Taste Buds ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Tactile Stimuli ◽  
Oral Sensory ◽  
Nerve Recordings

AbstractDuring development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.

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.

scholarly journals Intracellular free calcium oscillates during cell division of Xenopus embryos.

1991 ◽  
Vol 112 (4) ◽  
pp. 711-718 ◽  
Author(s):  
N Grandin ◽  
M Charbonneau
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Volume ◽  
Intracellular Ph ◽  
Calcium Ions ◽  
Volume Ratio ◽  
Mean Amplitude ◽  
Free Calcium ◽  
Periodic Oscillations ◽  
Xenopus Embryos

In Xenopus embryos, previous results failed to detect changes in the activity of free calcium ions (Ca2+i) during cell division using Ca2(+)-selective microelectrodes, while experiments with aequorin yielded uncertain results complicated by the variation during cell division of the aequorin concentration to cell volume ratio. We now report, using Ca2(+)-selective microelectrodes, that cell division in Xenopus embryos is accompanied by periodic oscillations of the Ca2+i level, which occur with a periodicity of 30 min, equal to that of the cell cycle. These Ca2+i oscillations were detected in 24 out of 35 experiments, and had a mean amplitude of 70 nM, around a basal Ca2+i level of 0.40 microM. Ca2+i oscillations did not take place in the absence of cell division, either in artificially activated eggs or in cleavage-blocked embryos. Therefore, Ca2+i oscillations do not represent, unlike intracellular pH oscillations (Grandin, N., and M. Charbonneau. J. Cell Biol. 111:523-532. 1990), a component of the basic cell cycle ("cytoplasmic clock" or "master oscillator"), but appear to be more likely related to some events of mitosis.

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