Possible Involvement of Undissociated Acid Molecules in the Acid Response of the Chorda Tympani Nerve of the Rat

2000 ◽  
Vol 83 (5) ◽  
pp. 2776-2779 ◽  
Author(s):  
Kazuma Ogiso ◽  
Yasutake Shimizu ◽  
Ken Watanabe ◽  
Keiichi Tonosaki
Keyword(s):  
Acetic Acid ◽  
Taste Receptor ◽  
Response Magnitude ◽  
Acid Solutions ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Weak Acids ◽  
Total Acid ◽  
Ph Dependent ◽  
Undissociated Acid

To test whether undissociated acid is capable of exciting the chorda tympani nerves in rats, we have used buffered acid solutions as taste stimuli. These solutions were prepared by adding alkali to weak acids, such as acetic acid, so that the proportion of undissociated and dissociated acids was varied whereas keeping the total acid concentration constant. When acetic acid solutions, adjusted to wide ranges of pH by NaOH, were applied to the tongue, the response magnitude of the chorda tympani nerves was not varied systematically with pH changes. However, if the sodium effect was eliminated by amiloride or replacement of cation by potassium or Tris[hydroxymethyl]aminomethane; NH2C(CH2OH)3 (Tris-base), the chorda tympani response was reduced systematically as pH increased. Similar results were obtained with citric acid and ascorbic acid. This pH-dependent change in taste nerve response to acid cannot be solely attributed to the proton gradient because the response magnitude induced by hydrogen itself, which was estimated from responses to strong acids, was much smaller than that by equi-pH acetic acid (∼85%). Thus we cannot explain the pH-dependent responses of the chorda tympani nerves to weak acids unless effects of undissociated acid molecules are postulated. It is therefore concluded that undissociated acids in weak acid solutions can be a stimulant to taste receptor cells.

Differential temperature dependence of taste nerve responses to various taste stimuli in dogs and rats

1991 ◽  
Vol 261 (6) ◽  
pp. R1402-R1408 ◽  
Author(s):  
M. Nakamura ◽  
K. Kurihara
Keyword(s):  
Acetic Acid ◽  
Temperature Dependence ◽  
Temperature Change ◽  
Dose Response ◽  
Monosodium Glutamate ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Response Curves ◽  
Tonic Response

The temperature dependence of the canine and rat chorda tympani nerve responses to various taste stimuli was examined. The temperature dependence greatly varied with species of stimuli. In the dog, the tonic responses to fructose, sucrose, acetic acid, and guanosine 5'-monophosphate (GMP) and the response induced by the synergism between monosodium glutamate (MSG) and GMP showed peaks at approximately 30 degrees C, whereas those to NaCl, NH4Cl, and MSG showed peaks between 10 and 20 degrees C. In the rat, the tonic response to NH4Cl increased with an increase in temperature up to 45 degrees C, whereas the responses to other stimuli examined showed peaks at approximately 30 degrees C. The responses to glycine, sucrose, and quinine showed sharp temperature dependence, and the responses to acids (HCl and acetic acid) and salts (NaCl and KCl) showed relatively flat dependence. The effects of the temperature change on dose-response curves for fructose, NH4Cl, and GMP were examined using dogs. The temperature change did not practically affect the thresholds for these stimuli and affected the magnitude of the responses to higher concentrations of stimuli. The origins of the temperature dependence were discussed in terms of taste receptor mechanisms.

scholarly journals Development of Rat Chorda Tympani Sodium Responses: Evidence for Age-Dependent Changes in Global Amiloride-Sensitive Na+Channel Kinetics

2000 ◽  
Vol 84 (3) ◽  
pp. 1531-1544 ◽  
Author(s):  
Susan J. Hendricks ◽  
Robert E. Stewart ◽  
Gerard L. Heck ◽  
John A. DeSimone ◽  
David L. Hill
Keyword(s):  
Kinetic Model ◽  
Maximum Rate ◽  
Taste Receptor ◽  
Taste Bud ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Channel Density ◽  
Age Dependent ◽  
Response Increase ◽  
Apical Membranes

In rat, chorda tympani nerve taste responses to Na+ salts increase between roughly 10 and 45 days of age to reach stable, mature magnitudes. Previous evidence from in vitro preparations and from taste nerve responses using Na+ channel blockers suggests that the physiological basis for this developmental increase in gustatory Na+ sensitivity is the progressive addition of functional, Na+ transduction elements (i.e., amiloride-sensitive Na+ channels) to the apical membranes of fungiform papilla taste receptor cells. To avoid potential confounding effects of pharmacological interventions and to permit quantification of aggregate Na+ channel behavior using a kinetic model, we obtained chorda tympani nerve responses to NaCl and sodium gluconate (NaGlu) during receptive field voltage clamp in rats aged from 12–14 to 60 days and older (60+ days). Significant, age-dependent increases in chorda tympani responses to these stimuli occurred as expected. Importantly, apical Na+ channel density, estimated from an apical Na+ channel kinetic model, increased monotonically with age. The maximum rate of Na+response increase occurred between postnatal days 12–14 and 29–31. In addition, estimated Na+ channel affinity increased between 12–14 and 19–23 days of age, i.e., on a time course distinct from that of the maximum rate of Na+response increase. Finally, estimates of the fraction of clamp voltage dropped across taste receptor apical membranes decreased between 19–23 and 29–31 days of age for NaCl but remained stable for NaGlu. The stimulus dependence of this change is consistent with a developmental increase in taste bud tight junctional Cl− ion permeability that lags behind the developmental increase in apical Na+ channel density. A significant, indirect anion influence on apical Na+ channel properties was present at all ages tested. This influence was evident in the higher apparent apical Na+ channel affinities obtained for NaCl relative to NaGlu. This stimulus-dependent modulation of apical Na+ channel apparent affinity relies on differences in the transepithelial potentials between NaCl and NaGlu. These originate from differences in paracellular anion permeability but act also on the driving force for Na+ through apical Na+channels. Detection of such an influence on taste depends fundamentally on the preservation of taste bud polarity and on a direct measure of sensory function, such as the response of primary afferents.

scholarly journals Acetic acid modulates spike rate and spike latency to salt in peripheral gustatory neurons of rats

2012 ◽  
Vol 108 (9) ◽  
pp. 2405-2418 ◽  
Author(s):  
Joseph M. Breza ◽  
Robert J. Contreras
Keyword(s):  
Acetic Acid ◽  
Artificial Saliva ◽  
Type I ◽  
Dependent Manner ◽  
Chorda Tympani ◽  
Gustatory System ◽  
Chorda Tympani Nerve ◽  
Concentration Dependent Manner ◽  
Lingual Epithelium ◽  
Taste Cells

Sour and salt taste interactions are not well understood in the peripheral gustatory system. Therefore, we investigated the interaction of acetic acid and NaCl on taste processing by rat chorda tympani neurons. We recorded multi-unit responses from the severed chorda tympani nerve (CT) and single-cell responses from intact narrowly tuned and broadly tuned salt-sensitive neurons in the geniculate ganglion simultaneously with stimulus-evoked summated potentials to signal when the stimulus contacted the lingual epithelium. Artificial saliva served as the rinse and solvent for all stimuli [0.3 M NH4Cl, 0.5 M sucrose, 0.1 M NaCl, 0.01 M citric acid, 0.02 M quinine hydrochloride (QHCl), 0.1 M KCl, 0.003–0.1 M acetic acid, and 0.003–0.1 M acetic acid mixed with 0.1 M NaCl]. We used benzamil to assess NaCl responses mediated by the epithelial sodium channel (ENaC). The CT nerve responses to acetic acid/NaCl mixtures were less than those predicted by summing the component responses. Single-unit analyses revealed that acetic acid activated acid-generalist neurons exclusively in a concentration-dependent manner: increasing acid concentration increased response frequency and decreased response latency in a parallel fashion. Acetic acid suppressed NaCl responses in ENaC-dependent NaCl-specialist neurons, whereas acetic acid-NaCl mixtures were additive in acid-generalist neurons. These data suggest that acetic acid attenuates sodium responses in ENaC-expressing-taste cells in contact with NaCl-specialist neurons, whereas acetic acid-NaCl mixtures activate distinct receptor/cellular mechanisms on taste cells in contact with acid-generalist neurons. We speculate that NaCl-specialist neurons are in contact with type I cells, whereas acid-generalist neurons are in contact with type III cells in fungiform taste buds.

Enhanced Responses of the Chorda Tympani Nerve to Sugars in the Ventromedial Hypothalamic Obese Rat

2003 ◽  
Vol 90 (1) ◽  
pp. 128-133 ◽  
Author(s):  
Yasutake Shimizu ◽  
Mifumi Yamazaki ◽  
Keiji Nakanishi ◽  
Maki Sakurai ◽  
Atsushi Sanada ◽  
...  
Keyword(s):  
Late Phase ◽  
Taste Receptor ◽  
Ventromedial Hypothalamus ◽  
Leptin Resistance ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
High Blood Glucose ◽  
Obesity And Diabetes ◽  
Significant Difference ◽  
Obese Rats

Sweet taste sensitivity in obese rats with lesions of the ventromedial hypothalamus (VMH) was studied by examining chorda tympani nerve responses to various taste stimuli including sugars. In the early progressive phase of obesity (2 wk after creating VMH lesions), there was no significant difference in the nerve responses to any taste stimulus between sham-operated and VMH-lesioned rats. In contrast, in the late phase of obesity (15–18 wk after VMH lesions), the magnitude of responses to sugars (except for fructose) was prominently greater than that in age-matched controls. High-fat diet-induced obese rats and streptozotocin-diabetic rats also showed greater chorda tympani nerve responses to sugars as was observed in VMH-lesioned obese rats, indicating that VMH lesions might not be specifically related to the enhanced gustatory neural responses to sugars. Although it has been demonstrated that the enhanced responses of the chorda tympani nerve to sugars in genetically diabetic db/db mice is largely attributable to the lack of the direct suppressive effect of leptin on the taste receptor cells, plasma leptin levels were not correlated with the changes in chorda tympani responsiveness to sugars in these models of obesity and diabetes. Accordingly, our results suggest that some chronic factors, including high blood glucose, inefficiency of insulin action, or leptin resistance may be related to the enhancement of chorda tympani nerve responses to sugars.

Modulation of rat chorda tympani nerve activity by lingual nerve stimulation

1995 ◽  
Vol 73 (4) ◽  
pp. 1468-1483 ◽  
Author(s):  
Y. Wang ◽  
R. P. Erickson ◽  
S. A. Simon
Keyword(s):  
Surface Temperature ◽  
Taste Receptor ◽  
Lingual Nerve ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Receptor System ◽  
Axon Reflex ◽  
Subcutaneous Injections ◽  
Peptide Release ◽  
Stimulation Voltage

1. A subpopulation of lingual nerve (LN) fibers surround and/or terminate in taste buds in fungiform papillae. One possible function of these fibers is to modulate chorda tympani fiber (CT) or taste responses. To test this hypothesis, the rat LN was stimulated electrically at various voltages (to 20 V), and single- and multiunit CT responses to water-0.1 M NaCl cycles were recorded before, during, and after LN stimulation. 2. When a thermally controlled water-0.1 M NaCl stimulus cycle was applied onto the tongue's surface, the surface temperature remained constant, independent of the stimulation voltage. In the absence of a liquid stimulus, the tongue's surface temperature increased approximately 4 degrees C upon LN stimulation for voltages > or = 5 V. This temperature increase, caused by vasodilation by way of the axon reflex flare mechanism, was taken as evidence that LN stimulation induces peptide release. 3. Comparison of CT activity before LN stimulation with the activity either during or after stimulation revealed statistically significant changes in CT activity. During LN stimulation the CT activity decreased. After LN stimulation, the variability in amount of CT activity increased. 4. In rats treated postnatally with subcutaneous injections of capsaicin to reduce or eliminate polymodal nociceptors, LN stimulation did not produce increases in the tongue's surface temperature or changes in CT activity. 5. Changes in CT activity could be detected seconds after LN stimulation, suggesting that the intragemmal and/or perigemmal LN fibers modulate CT activity. 6. The physiological implications of this study suggest that CT responses to salt can be modulated by endogenous compounds (probably peptides), eating foods that activate LN responses (e.g., foods that are very acidic or contain capsaicin) may modulate taste responses, and peri- and intragemmal fibers should be considered an integral part of the taste receptor system.

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.

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.

Responses of gustatory cells in the nucleus of the solitary tract of the hamster after NaCl or amiloride adaptation

1996 ◽  
Vol 76 (1) ◽  
pp. 47-58 ◽  
Author(s):  
D. V. Smith ◽  
H. Liu ◽  
M. B. Vogt
Keyword(s):  
Taste Receptor ◽  
Chorda Tympani ◽  
Solitary Tract ◽  
Chorda Tympani Nerve ◽  
Receptor Cells ◽  
Human Tongue ◽  
Baseline Response ◽  
Single Nucleus ◽  
Adaptation Condition ◽  
Stimulus Classification

1. The responses of single nucleus of the solitary tract (NST) neurons in the hamster were recorded to an array of Na+ and non-Na+ stimuli under each of three adaptation conditions: distilled H2O, 0.032 M NaCl, and 10 microM amiloride. Each adapting solution flowed for 60 s before delivery of one of seven test stimuli: 0.032 M NaCl, NaNO3, and Na-gluconate, 0.1 M KCl and sucrose, 1 mM HCl, and 3 mM quinine hydrochloride (QHCl). Stimuli were dissolved in distilled H2O (H2O and NaCl adaptation conditions) or 10 microM amiloride (amiloride adaptation condition). 2. Both amiloride treatment and NaCl adaptation reduced responses to the Na+ stimuli. The effects of NaCl adaptation were generally greater than those of amiloride, and the responses to the Na+ salts were reduced by NaCl adaptation in every cell that responded to NaCl, regardless of its best-stimulus classification. Amiloride treatment suppressed the responses to Na+ salts with larger anions (NaNO3 and Na-gluconate) more than the response to NaCl. 3. Unlike amiloride treatment, NaCl adaptation also reduced responses to several non-Na+ stimuli (KCl, HCl, and QHCl). This effect occurred primarily in the NaCl-best neurons that were most highly responsive to NaCl and that showed a postexcitatory suppression after NaCl. This suppression has been observed in recordings from the chorda tympani nerve in both rats and hamsters and in taste receptor cell responses recorded in situ in the rat. If it is a receptor phenomenon, these data would imply that some NaCl-sensitive receptor cells are also responsive to these non-Na+ electrolytes. 4. The effects of amiloride on the responses to Na+ stimuli were not limited to NaCl-best neurons, but occurred in sucrose-best cells as well. These results suggest that the sucrose-best cells in the NST receive converging input from sucrose- and NaCl-best chorda tympani fibers, because there is little Na+ sensitivity in the peripheral sucrose-best fibers and the amiloride sensitivity is restricted to NaCl-best chorda tympani fibers. The responses to NaCl in the few HCl- and QHCl-best NST neurons were not affected by amiloride. 5. Rinsing the tongue with amiloride for 60 s resulted in a reduction in the baseline response rate of NST cells. This effect occurred primarily in NaCl- and sucrose-best NST neurons and implies that much of the spontaneous activity in these brain stem cells arises from amiloride-sensitive channel activity in the peripheral receptor cells. 6. The results of human psychophysical studies show very different effects of NaCl adaptation and amiloride treatment. Adaptation to NaCl produces a robust and specific reduction in the saltiness of all salts. The present results show that NaCl adaptation reduces the responses of all cells sensitive to NaCl. Treatment of the human tongue with amiloride produces a proportionately smaller reduction in the response to NaCl than it does in rodents, and it appears to have no effect on saltiness. Rather, amiloride has been shown to specifically reduce the sour side taste of NaCl, Nagluconate, and LiCl. Therefore conclusions about the effects of amiloride on taste quality based on rodent electrophysiology are questionable.

An analysis of the time course of gustatory neural adaptation in the rat

1975 ◽  
Vol 229 (4) ◽  
pp. 1134-1140 ◽  
Author(s):  
DV Smith ◽  
JW Steadman ◽  
CN Rhodine
Keyword(s):  
Transient Response ◽  
Time Course ◽  
Taste Receptor ◽  
Constant Term ◽  
Fast Time ◽  
Adaptation Process ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Nacl Concentration ◽  
Neural Discharge

Neural responses were recorded from the rat chorda tympani nerve following stimulation of the tongue with several concentrations of NaCl. These responses were integrated using a fast time constant (47 ms), and the time course of the decline in neural discharge from the peak of the transient response was computer analyzed. The time course of the adaptation process was described by a constant term and two exponentially decaying components, which most likely reflect the existence of two separate mechanisms contributing to the adaptation process in taste. The constant term and the amplitude of the second gradual exponential decay were correlated with NaCl concentration, whereas the amplitude of the initial rapidly declining exponential component was independent of stimulus intensity. The initial transient response of the chorda tympani nerve may be a function of the rate of stimulus adsorption, whereas the gradual second decline in the neural response may reflect an adaptive mechanism of the taste receptor cell.

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