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 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.

Sweet Taste Responses of Mouse Chorda Tympani Neurons: Existence of Gurmarin-Sensitive and -Insensitive Receptor Components

1999 ◽  
Vol 81 (6) ◽  
pp. 3087-3091 ◽  
Author(s):  
Yuzo Ninomiya ◽  
Toshiaki Imoto ◽  
Tadataka Sugimura
Keyword(s):  
Sweet Taste ◽  
The Other ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Inhibitory Effects ◽  
Single Fibers ◽  
Taste Cells ◽  
C57bl Mice ◽  
Mouse Taste

Sweet taste responses of mouse chorda tympani neurons: existence of gurmarin-sensitive and -insensitive receptor components. Inhibitory effects of gurmarin (gur) on responses to sucrose and other sweeteners of single fibers of the chorda tympani nerve in C57BL mice were examined. Of 30 single fibers that strongly responded to 0.5 M sucrose but were not or to lesser extent responsive to 0.1 M NaCl, 0.01 M HCl, and 0.02 M quinine HCl (sucrose-best fibers), 16 fibers showed large suppression of responses to sucrose and other sweeteners by lingual treatment with 4.8 μM (∼20 μg/ml) gur (suppressed to 4–52% of control: gur-sensitive fibers), whereas the remaining 14 fibers showed no such gur inhibition (77–106% of control: gur-insensitive fibers). In gur-sensitive fibers, responses to sucrose inhibited by gur recovered to ∼70% of control responses after rinsing the tongue with 15 mM β-cyclodextrin and were almost abolished by further treatment with 2% pronase. In gur-insensitive fibers, sucrose responses were not inhibited by gur, but were largely suppressed by pronase. These results suggest existence of two different receptor components for sweeteners with different susceptibilities to gur in mouse taste cells, one gur sensitive and the other gur insensitive. Taste cells possessing each component may be specifically innervated by a particular type of chorda tympani neurons.

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.

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.

Taste Buds and Gustatory Transduction: A Functional Perspective

2021 ◽  
Author(s):  
Alan C. Spector ◽  
Susan P. Travers
Keyword(s):  
Expression Profiles ◽  
Cranial Nerves ◽  
Taste Receptor ◽  
Taste Buds ◽  
Taste Bud ◽  
Type I ◽  
Gustatory System ◽  
Type Iii ◽  
Functional Perspective ◽  
The Brain

Everything a person swallows must pass a final chemical analysis by the sensory systems of the mouth; of these, the gustatory system is cardinal. Gustation can be heuristically divided into three basic domains of function: sensory-discriminative (quality and intensity), motivational/affective (promote or deter ingestion), and physiological (e.g., salivation and insulin release). The signals from the taste buds, transmitted to the brain through the sensory branches of cranial nerves VII (facial), IX (glossopharyngeal), and X (vagal), subserve these primary functions. Taste buds are collections of 50–100 cells that are distributed in various fields in the tongue, soft palate, and throat. There are three types of cells that have been identified in taste buds based on their morphological and cytochemical expression profiles. Type II cells express specialized G-protein-coupled receptors (GPCR or GPR) on their apical membranes, which protrude through a break in the oral epithelial lining called the taste pore, that are responsible for the sensing of sweeteners (via the taste type 1 receptor (T1R) 2 + T1R3), amino acids (via the T1R1+T1R3), and bitter ligands (via the taste type 2 receptors (T2Rs)). Type III cells are critical for the sensing of acids via the otopetrin-1 (Otop-1) ion channel. The sensing of sodium, in at least rodents, occurs through the epithelial sodium channel (ENaC), but the exact composition of this channel and the type of taste cell type in which the functional version resides remains unclear. It is controversial whether Type I cells, which have been characterized as glial-like, are involved in sodium transduction or play any taste signaling role. For the most part, receptors for different stimulus classes (e.g., sugars vs. bitter ligands) are not co-expressed, providing significant early functionally related segregation of signals. There remains a persistent search for yet to be identified receptors that may contribute to some functions associated with stimuli representing the so-called basic taste qualities—sweet, salty, sour, bitter, and umami—as well as unconventional stimuli such as fatty acids (in addition to cluster of differentiation-36 (CD-36), GPR40, and GPR120) and maltodextrins. The primary neurotransmitter in taste receptor cells is ATP, which is released through a voltage-gated heteromeric channel consisting of the calcium homeostasis modulator 1 and 3 (CALHM1/3) and binds with P2X2/X3 receptors on apposed afferent fibers. Serotonin released from Type III cells has been implicated as an additional neurotransmitter, binding with HT3a receptors, and possibly playing a role in acid taste (which is sour to humans). Taste bud cells undergo complete turnover about every two weeks. Although there remains much to be understood about the operations of the taste bud, perhaps the one very clear principle that emerges is that the organization of signals transmitted to the brain is not random and arbitrary to be decoded by complex algorithms in the circuits of the central gustatory system. Rather, the transmission of taste information from the periphery is highly ordered.

scholarly journals Anion modulation of taste responses in sodium-sensitive neurons of the hamster chorda tympani nerve.

1993 ◽  
Vol 101 (3) ◽  
pp. 453-465 ◽  
Author(s):  
B G Rehnberg ◽  
B I MacKinnon ◽  
T P Hettinger ◽  
M E Frank
Keyword(s):  
Nerve Fibers ◽  
Na Channel ◽  
Acetate Anion ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Wide Range ◽  
Nacl Concentration ◽  
Stimulus Concentration ◽  
Taste Cells ◽  
Epithelial Membranes

Beidler's work in the 1950s showed that anions can strongly influence gustatory responses to sodium salts. We have demonstrated "anion inhibition" in the hamster by showing that the chorda tympani nerve responds more strongly to NaCl than to Na acetate over a wide range of concentrations. Iontophoretic presentation of Cl- and acetate to the anterior tongue elicited no response in the chorda tympani, suggesting that these anions are not directly stimulatory. Drugs (0.01, 1.0, and 100 microM anthracene-9-carboxylate, diphenylamine-2-carboxylate, 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonate, and furosemide) that interfere with movements of Cl- across epithelial cells were ineffective in altering chorda tympani responses to 0.03 M of either NaCl or Na acetate. Anion inhibition related to movements of anions across epithelial membranes therefore seems unlikely. The chorda tympani contains a population of nerve fibers highly selective for Na+ (N fibers) and another population sensitive to Na+ as well as other salts and acids (H fibers). We found that N fibers respond similarly to NaCl and Na acetate, with spiking activity increasing with increasing stimulus concentration (0.01-1.0 M). H fibers, however, respond more strongly to NaCl than to Na acetate. Furthermore, H fibers increase spiking with increases in NaCl concentration, but generally decrease their responses to increasing concentrations of Na acetate. It appears that anion inhibition applies to taste cells innervated by H fibers but not by N fibers. Taste cells innervated by N fibers use an apical Na+ channel, whereas those innervated by H fibers may use a paracellularly mediated, basolateral site of excitation.

Sign in / Sign up

Export Citation Format

Share Document