scholarly journals Recovery of Salt Taste Responses and PGP 9.5 Immunoreactive Taste Bud Cells during Regeneration of the Mouse Chorda Tympani Nerve

2005 ◽  
Vol 30 (Supplement 1) ◽  
pp. i62-i63 ◽  
Author(s):  
K. Yasumatsu
Keyword(s):  
Taste Bud ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Pgp 9.5 ◽  
Salt Taste ◽  
Taste Bud Cells

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.

Salt taste discrimination after bilateral section of the chorda tympani or glossopharyngeal nerves

1992 ◽  
Vol 263 (1) ◽  
pp. R169-R176 ◽  
Author(s):  
A. C. Spector ◽  
H. J. Grill
Keyword(s):  
Discrimination Performance ◽  
Taste Buds ◽  
Glossopharyngeal Nerve ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Critical Elements ◽  
Electrophysiological Findings ◽  
Taste Discrimination ◽  
Salt Taste Discrimination

Gustatory deafferentation of the anterior tongue by bilateral section of the chorda tympani nerve, which removes only 15% of the total taste buds in the rat, severely impaired the rat's ability to discriminate NaCl from KCl. The discrimination deficit was selective. Denervated rats were able to discriminate sucrose from quinine. Despite eliminating four times as many taste buds by bilateral section of the glossopharyngeal nerve, posterior lingual deafferentation had no effect on NaCl vs. KCl discrimination performance. Collectively, these data suggest that afferents in the chorda tympani nerve provide the highest degree of disparity between the peripheral signals representing NaCl and KCl. Electrophysiological findings of others implicate the sodium-specific afferents that appear to exclusively exist in the chorda tympani nerve as the critical elements subserving the NaCl vs. KCl discrimination.

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.

scholarly journals Effects of voltage perturbation of the lingual receptive field on chorda tympani responses to Na+ and K+ salts in the rat: implications for gustatory transduction.

1994 ◽  
Vol 104 (5) ◽  
pp. 885-907 ◽  
Author(s):  
Q Ye ◽  
G L Heck ◽  
J A DeSimone
Keyword(s):  
Receptive Field ◽  
Voltage Clamp ◽  
Maximal Response ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Negative Voltage ◽  
Voltage Clamp Condition ◽  
Taste Cells ◽  
Clamp Condition

Taste sensory responses from the chorda tympani nerve of the rat were recorded with the lingual receptive field under current or voltage clamp. Consistent with previous results (Ye, Q., G. L. Heck, and J. A. DeSimone. 1993. Journal of Neurophysiology. 70:167-178), responses to NaCl were highly sensitive to lingual voltage clamp condition. This can be attributed to changes in the electrochemical driving force for Na+ ions through apical membrane transducer channels in taste cells. In contrast, responses to KCl over the concentration range 50-500 mM were insensitive to the voltage clamp condition of the receptive field. These results indicate the absence of K+ conductances comparable to those for Na+ in the apical membranes of taste cells. This was supported by the strong anion dependence of K salt responses. At zero current clamp, the potassium gluconate (KGlu) threshold was > 250 mM, and onset kinetics were slow (12 s to reach half-maximal response). Faster onset kinetics and larger responses to KGlu occurred at negative voltage clamp (-50 mV). This indicates that when K+ ion is transported as a current, and thereby uncoupled from gluconate mobility, its rate of delivery to the K+ taste transducer increases. Analysis of conductances shows that the paracellular pathway in the lingual epithelium is 28 times more permeable to KCl than to KGlu. Responses to KGlu under negative voltage clamp were not affected by agents that are K+ channel blockers in other systems. The results indicate that K salt taste transduction is under paracellular diffusion control, which limits chemoreception efficiency. We conclude that rat K salt taste occurs by means of a subtight junctional transducer for K+ ions with access limited by anion mobility. The data suggest that this transducer is not cation selective which also accounts for the voltage and amiloride insensitive part of the response to NaCl.

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.

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.

Enhancement of gustatory nerve fibers to NaCl and formation of ion channels by commercial novobiocin

1994 ◽  
Vol 266 (5) ◽  
pp. C1165-C1172 ◽  
Author(s):  
A. M. Feigin ◽  
Y. Ninomiya ◽  
S. M. Bezrukov ◽  
B. P. Bryant ◽  
P. A. Moore ◽  
...  
Keyword(s):  
Ion Channels ◽  
Lipid Bilayers ◽  
Neutral Lipids ◽  
Nerve Fibers ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Cation Selectivity ◽  
Taste Response ◽  
Gustatory Nerve

Single fibers of the rat chorda tympani nerve were used to study the mechanism of action of the antibiotic novobiocin on salt taste transduction. In the rat, novobiocin selectively enhanced the responses of sodium-specific and amiloride-sensitive chorda tympani nerve fibers (N type) without affecting more broadly responsive cation-sensitive and amiloride-insensitive fibers (E type). In the presence of amiloride, novobiocin was ineffective at enhancing the response of N-type fibers toward sodium chloride. Novobiocin also increased the conductance of bilayers formed from neutral lipids by forming nonrectifying ion channels with low conductance (approximately 7 pS in 110 mM NaCl), long open times (several seconds and longer), and high cation selectivity. Amiloride did not alter either the conductance or kinetics of these novobiocin channels. These observations suggest that even though novobiocin is able to form cation channels in lipid bilayers, and possibly in cell membranes as well, its action on the salt-taste response is through modulation of existing amiloride-sensitive sodium channels.

scholarly journals Contribution of the TRPV1 channel to salt taste quality in mice as assessed by conditioned taste aversion generalization and chorda tympani nerve responses

2012 ◽  
Vol 303 (11) ◽  
pp. R1195-R1205 ◽  
Author(s):  
Kimberly R. Smith ◽  
Yada Treesukosol ◽  
A. Brennan Paedae ◽  
Robert J. Contreras ◽  
Alan C. Spector
Keyword(s):  
Citric Acid ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Taste Quality ◽  
Transient Receptor Potential Vanilloid ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Trpv1 Channel ◽  
Salt Taste ◽  
Transient Receptor

In rodents, at least two transduction mechanisms are involved in salt taste: 1) the sodium-selective epithelial sodium channel, blocked by topical amiloride administration, and 2) one or more amiloride-insensitive cation-nonselective pathways. Whereas electrophysiological evidence from the chorda tympani nerve (CT) has implicated the transient receptor potential vanilloid-1 (TRPV1) channel as a major component of amiloride-insensitive salt taste transduction, behavioral results have provided only equivocal support. Using a brief-access taste test, we examined generalization profiles of water-deprived C57BL/6J (WT) and TRPV1 knockout (KO) mice conditioned (via LiCl injection) to avoid 100 μM amiloride-prepared 0.25 M NaCl and tested with 0.25 M NaCl, sodium gluconate, KCl, NH4Cl, 6.625 mM citric acid, 0.15 mM quinine, and 0.5 M sucrose. Both LiCl-injected WT and TRPV1 KO groups learned to avoid NaCl+amiloride relative to controls, but their generalization profiles did not differ; LiCl-injected mice avoided the nonsodium salts and quinine suggesting that a TRPV1-independent pathway contributes to the taste quality of the amiloride-insensitive portion of the NaCl signal. Repeating the experiment but doubling all stimulus concentrations revealed a difference in generalization profiles between genotypes. While both LiCl-injected groups avoided the nonsodium salts and quinine, only WT mice avoided the sodium salts and citric acid. CT responses to these stimuli and a concentration series of NaCl and KCl with and without amiloride did not differ between genotypes. Thus, in our study, TRPV1 did not appear to contribute to sodium salt perception based on gustatory signals, at least in the CT, but may have contributed to the oral somatosensory features of sodium.

scholarly journals Effect of Chorda Tympani Nerve Transection on Salt Taste Perception in Mice

2011 ◽  
Vol 36 (9) ◽  
pp. 811-819 ◽  
Author(s):  
G. J. Golden ◽  
Y. Ishiwatari ◽  
M. L. Theodorides ◽  
A. A. Bachmanov
Keyword(s):  
Taste Perception ◽  
Chorda Tympani ◽  
Nerve Transection ◽  
Chorda Tympani Nerve ◽  
Salt Taste

scholarly journals Hedgehog pathway blockade with the cancer drug LDE225 disrupts taste organs and taste sensation

2015 ◽  
Vol 113 (3) ◽  
pp. 1034-1040 ◽  
Author(s):  
Archana Kumari ◽  
Alexandre N. Ermilov ◽  
Benjamin L. Allen ◽  
Robert M. Bradley ◽  
Andrzej A. Dlugosz ◽  
...  
Keyword(s):  
Basal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Basal Cell ◽  
Taste Buds ◽  
Taste Bud ◽  
Chorda Tympani ◽  
Taste Sensation ◽  
Chorda Tympani Nerve ◽  
Receptor Cells ◽  
Hh Signaling

Taste sensation on the anterior tongue requires chorda tympani nerve function and connections with continuously renewing taste receptor cells. However, it is unclear which signaling pathways regulate the receptor cells to maintain chorda tympani sensation. Hedgehog (HH) signaling controls cell proliferation and differentiation in numerous tissues and is active in taste papillae and taste buds. In contrast, uncontrolled HH signaling drives tumorigenesis, including the common skin cancer, basal cell carcinoma. Systemic HH pathway inhibitors (HPIs) lead to basal cell carcinoma regression, but these drugs cause severe taste disturbances. We tested the hypothesis that taste disruption by HPIs reflects a direct requirement for HH signaling in maintaining taste organs and gustatory sensation. In mice treated with the HPI LDE225 up to 28 days, HH-responding cells were lost in fungiform papilla epithelium, and papillae acquired a conical apex. Taste buds were either absent or severely reduced in size in more than 90% of aberrant papillae. Taste bud remnants expressed the taste cell marker keratin 8, and papillae retained expression of nerve markers, neurofilament and P2X3. Chorda tympani nerve responses to taste stimuli were markedly reduced or absent in LDE225-treated mice. Responses to touch were retained, however, whereas cold responses were retained after 16 days of treatment but lost after 28 days. These data identify a critical, modality-specific requirement for HH signaling in maintaining taste papillae, taste buds and neurophysiological taste function, supporting the proposition that taste disturbances in HPI-treated patients are an on-target response to HH pathway blockade in taste organs.

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