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 ENaC-Dependent Sodium Chloride Taste Responses in the Regenerated Rat Chorda Tympani Nerve After Lingual Gustatory Deafferentation Depend on the Taste Bud Field Reinnervated

2020 ◽  
Vol 45 (4) ◽  
pp. 249-259
Author(s):  
Enshe Jiang ◽  
Ginger D Blonde ◽  
Mircea Garcea ◽  
Alan C Spector
Keyword(s):  
Taste Receptor ◽  
Taste Bud ◽  
Male Rats ◽  
Electrophysiological Recording ◽  
Na Channel ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Response Properties ◽  
Gustatory Nerve ◽  
The Cross

Abstract The chorda tympani (CT) nerve is exceptionally responsive to NaCl. Amiloride, an epithelial Na+ channel (ENaC) blocker, consistently and significantly decreases the NaCl responsiveness of the CT but not the glossopharyngeal (GL) nerve in the rat. Here, we examined whether amiloride would suppress the NaCl responsiveness of the CT when it cross-reinnervated the posterior tongue (PT). Whole-nerve electrophysiological recording was performed to investigate the response properties of the intact (CTsham), regenerated (CTr), and cross-regenerated (CT-PT) CT in male rats to NaCl mixed with and without amiloride and common taste stimuli. The intact (GLsham) and regenerated (GLr) GL were also examined. The CT responses of the CT-PT group did not differ from those of the GLr and GLsham groups, but did differ from those of the CTr and CTsham groups for some stimuli. Importantly, the responsiveness of the cross-regenerated CT to a series of NaCl concentrations was not suppressed by amiloride treatment, which significantly decreased the response to NaCl in the CTr and CTsham groups and had no effect in the GLr and GLsham groups. This suggests that the cross-regenerated CT adopts the taste response properties of the GL as opposed to those of the regenerated CT or intact CT. This work replicates the 5 decade-old findings of Oakley and importantly extends them by providing compelling evidence that the presence of functional ENaCs, essential for sodium taste recognition in regenerated taste receptor cells, depends on the reinnervated lingual region and not on the reinnervating gustatory nerve, at least in the rat.

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 Optogenetic Activation of Type III Taste Cells Modulates Taste Responses

2020 ◽  
Vol 45 (7) ◽  
pp. 533-539
Author(s):  
Aurelie Vandenbeuch ◽  
Courtney E Wilson ◽  
Sue C Kinnamon
Keyword(s):  
Light Response ◽  
Sensory Nerves ◽  
Taste Bud ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Type Iii ◽  
Nonspecific Effects ◽  
Taste Cells ◽  
Specific Stimulation ◽  
The Brain

Abstract Studies have suggested that communication between taste cells shapes the gustatory signal before transmission to the brain. To further explore the possibility of intragemmal signal modulation, we adopted an optogenetic approach to stimulate sour-sensitive (Type III) taste cells using mice expressing Cre recombinase under a specific Type III cell promoter, Pkd2l1 (polycystic kidney disease-2-like 1), crossed with mice expressing Cre-dependent channelrhodopsin (ChR2). The application of blue light onto the tongue allowed for the specific stimulation of Type III cells and circumvented the nonspecific effects of chemical stimulation. To understand whether taste modality information is preprocessed in the taste bud before transmission to the sensory nerves, we recorded chorda tympani nerve activity during light and/or chemical tastant application to the tongue. To assess intragemmal modulation, we compared nerve responses to various tastants with or without concurrent light-induced activation of the Type III cells. Our results show that light significantly decreased taste responses to sweet, bitter, salty, and acidic stimuli. On the contrary, the light response was not consistently affected by sweet or bitter stimuli, suggesting that activation of Type II cells does not affect nerve responses to stimuli that activate Type III cells.

Enhanced membrane turnover in response to stimuli in the primate taste bud

1989 ◽  
Vol 47 ◽  
pp. 788-789
Author(s):  
Albert I. Farbman ◽  
Göran Hellekant
Keyword(s):  
Rhesus Monkeys ◽  
Nerve Impulse ◽  
Salivary Secretion ◽  
Taste Bud ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Membrane Turnover ◽  
Fungiform Papilla ◽  
Thin Sections ◽  
Receptor Complexes

The presence of membrane-enclosed vesicles, 50-100 nm in diameter (cf. Fig. 1), has been observed in the taste pores of rats, mice, and rabbits, although little attention has been devoted to their importance. Murray has noted that fungiform papilla taste pores contained more vesicles than foliate papilla pores. In a recent paper we showed that thaumatin, an intensely sweet, basic protein (pl = 12), binds to the vesicles and to microvilli in taste pores. We suggested that the vesicles were shed from the microvilli as a kind of apocrine secretion, and proposed that the shedding of these vesicles may be an important means by which taste bud cells rid themselves of certain stimulus/receptor complexes, particularly when the stimulus is a large and/or highly charged molecule, such as thaumatin. To investigate this hypothesis further, we used electron microscopy to examine taste pores of both vallate and foliate papillae from Rhesus monkeys, before and after stimulation with thaumatin. We also recorded neural activity from the glossopharyngeal and chorda tympani nerves during stimulation with thaumatin and other tastants.Rhesus monkeys were anesthetized with ketamine and given glycopyrrolate to inhibit salivary secretion. Tongues were thoroughly rinsed and the region of the foliate or vallate papilla treated with thaumatin (33 mg/1) or sucrose (0.3M) for 5-10 min. After a brief rinse, papillae were removed surgically. Control papillae were biopsied with no stimulation. Specimens were fixed for 2 h in: 2% paraformaldehyde, 2% glutaraldehyde in phosphate buffer, pH 7.2, rinsed and post-fixed in phosphate-buffered 1% OsO4,dehydrated in ethanols, and embedded in Epon-Araldite. Thin sections were examined in a JEOL-100 CX electron microscope with particular attention to the contents of the taste pores. For neurophysiology, the glossopharyngeal or chorda tympani nerve was exposed, in anesthetized monkeys, by dissection, and electrodes were placed on the nerve. Impulse activity was recorded with a PAR 113 amplifier, monitored over a loudspeaker and an oscilloscope, and fed into a recorder together with the output from an integrator which indicated the type and time of stimulation. The tongue was stimulated with a system that delivers solutions at programmed intervals under conditions of constant flow and temperature. Each stimulation lasted 10 sec, followed by a 30 or 50 sec rinse before the next stimulus. Stimuli were 0.02M citric acid, 0.1 M NaCl, 0.3M sucrose and 33 mg/l thaumatin.

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.

Chemospecific deficits in taste detection after selective gustatory deafferentation in rats

1990 ◽  
Vol 258 (3) ◽  
pp. R820-R826 ◽  
Author(s):  
A. C. Spector ◽  
G. J. Schwartz ◽  
H. J. Grill
Keyword(s):  
Detection Threshold ◽  
Conditioned Avoidance ◽  
Taste Bud ◽  
Taste Receptors ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Before And After ◽  
The Mean ◽  
Taste Detection ◽  
Response To Water

Electrophysiological data support the existence of sodium-specific taste receptors that appear to be limited to the anterior tongue. However, previous behavioral findings suggest that bilateral transection of the chorda tympani nerve (CTn) has minimal consequences on NaCl intake and preference. This study employed a conditioned avoidance procedure to measure detection thresholds to NaCl and sucrose both before and after bilateral transection of the CTn. Rats were trained to maintain spout contact in response to water presentations (70 microliters) and to avoid spout contact when a taste solution (70 microliters) was presented. In experiment 1, all rats (n = 3) showed statistically significant impairments in the detectability of NaCl after bilateral section of the CTn. The mean increase in the NaCl detection threshold was 1.41 log units. In contrast, sucrose threshold in these same rats was marginally affected by CTn section (mean increase = 0.22 log units). Experiment 2 (n = 4) replicated the findings of the first experiment. The mean increase in the NaCl detection threshold was 2.23 log units. Sucrose threshold in these rats was, again, only marginally affected by CTn section (mean increase = 0.83 log units). Histological examination of the anterior tongue from the rats in experiment 2 indicated that the CTn transections were complete. These findings reveal that the anterior oral receptive field (innervated by the CTn) containing only 15% of the total taste bud population is critical for the normal detection of NaCl.

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