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PubMed1997

Broad tuning of rat taste cells for four basic taste stimuli.

The breadth of responsiveness of rat taste cells to the four basic taste stimuli was studied using the entropy measure (H) proposed by Smith and Travers. H values range from 0.0 for narrow tuning to 1.0 for broad tuning. Based on the responses of depolarizing receptor potentials of 26 rat taste cells to the four basic taste stimuli, taste cells were classified into nine NaCl-best, four Q-HCl (quinine-HCl)-best, 10 HCl-best and three sucrose-best cells. NaCl-best cells were narrowly tuned to the four basic taste stimuli, but the other three stimuli-best cells were broadly tuned to the stimuli. In all, 85% of the taste cells responded to more than one of four basic taste stimuli. The mean H values for NaCl-best, Q-HCl-best, HCl-best and sucrose-best cells were 0.285, 0.832, 0.781 and 0.796 respectively. The mean H value for all 26 taste cells was 0.621. This was larger than H in rat gustatory fibers. Transformation of large H values in taste cells into small H values in taste fibers may be due to a non-random interaction between taste cells and taste fibers during the synaptic formation. Broad tuning properties of rat taste cells suggest that the across-taste cell response pattern may play an important role in taste quality coding mechanisms.

Animals↗
PubMed1988

Ultrastructure of mouse foliate taste buds: synaptic and nonsynaptic interactions between taste cells and nerve fibers.

High voltage electron microscopy and conventional transmission electron microscopy were used to examine the ultrastructure of foliate taste buds of mice. Computer-assisted, three-dimensional reconstructions from serial sections were used to visualize regions of interaction between taste cells and nerve fibers. Based on criteria previously established for murine vallate taste buds (Kinnamon et al., '85), foliate taste cells were classified as dark, light, or intermediate depending on their cytoplasmic content and the characteristics of their nuclei. Cells of foliate taste buds display a continuous range of morphologies, from "typical" dark cells to "typical" light cells. Cells of dark, intermediate, and light morphologies all make afferent synapses onto nerve processes, suggesting that cells of all 3 types are sensory in function. Synapses between taste cells and nerve processes may be either macular or fingerlike in shape. No efferent synapses were found. In addition to conventional synapses, taste cells exhibit 2 other types of specializations at sites of apposition with nerve fibers: subsurface cisternae and atypical mitochondria. Subsurface cisternae are narrow sacs of endoplasmic reticulum that are closely apposed to the inner leaflet of the taste cell membrane. Possible functions of subsurface cisternae include synthesis of synaptic membrane components, modification of the electrical or adhesive properties of the taste cell membrane, and exchange of trophic factors with nerve processes. Atypical mitochondria are usually much larger than typical taste cell mitochondria, and their cristae often display a swollen, twisted configuration. These mitochondria are closely apposed to the inside of the taste cell membrane adjacent to nerve fibers. Atypical mitochondria may be providing unusual amounts of energy for metabolic reactions in their vicinities or participating in calcium buffering in the taste cell. Within taste cells, presynaptic specializations, subsurface cisternae, and mitochondria are often clustered together to form "synaptic ensembles." We hypothesize that the functions served by the subsurface cisternae and mitochondria, as well as synaptic transmission, may be important in interactions between taste cells and nerve fibers.

Animals↗
PubMed2005

Molecular definition of black tea taste by means of quantitative studies, taste reconstitution, and omission experiments.

Recently, bioresponse-guided fractionation of black tea infusions indicated that neither the high molecular weight thearubigens nor the theaflavins, but a series of 14 flavon-3-ol glycopyranosides besides some catechins, might be important contributors to black tea taste. To further bridge the gap between pure structural chemistry and human taste perception, in the present investigation 51 putative taste compounds have been quantified in a black tea infusion, and their dose-over-threshold (Dot) factors have been calculated on the basis of a dose/threshold relationship. To confirm these quantitative results, an aqueous taste model was prepared by blending aqueous solutions of 15 amino acids, 14 flavonol-glycosides, 8 flavan-3-ols, 5 theaflavins, 5 organic acids, 3 sugars, and caffeine in their "natural" concentrations. Sensory analyses revealed that the taste profile of this artificial cocktail did not differ significantly from the taste profile of the authentic tea infusion. To further narrow the number of key taste compounds, finally, taste omission experiments have been performed, on the basis of which a reduced recombinate was prepared containing the bitter-tasting caffeine, nine velvety astringent flavonol-3-glycosides, and the puckering astringent catechin as well as the astringent and bitter epigallocatechin-3-gallate. The taste profile of this reduced recombinate differed not significantly from that of the complete taste recombinate, thus confirming these 12 compounds as the key taste compounds of the tea infusion. Additional sensory studies demonstrated for the first time that the flavanol-3-glycosides not only impart a velvety astringent taste sensation to the oral cavity but also contribute to the bitter taste of tea infusions by amplifying the bitterness of caffeine.

Amino Acids↗
PubMed2004

Glutamate taste: Discrimination between the tastes of glutamate agonists and monosodium glutamate in rats.

Taste aversion studies have demonstrated that rats conditioned to avoid monosodium glutamate (MSG) with amiloride added to reduce the intensity of the sodium component of MSG taste, generalize this aversion to aspartic acid and to L-AP4, but not to ionotropic glutamate receptor agonists. That is, MSG, L-AP4 and aspartate have similar tastes to rats. However, conditioned taste aversion methods are unable to show to what extent the tastes of two substances are different. If two substances activate the same afferent processes (e.g. taste receptors), they are likely to produce the same tastes, but if they activate different afferent processes, the subject may detect differences between the tastes of the substances. In this study, rats were tested to determine if they could discriminate between the tastes of these agonists and MSG. We also established the detection thresholds for NMDA, aspartic acid and L-AP4, with and without amiloride (a sodium channel antagonist). Taste threshold values were 1-4 mM for NMDA and aspartic acid and 0.5-2.5 microM for L-AP4. None were affected by 30 micro M amiloride. Rats could readily distinguish between the tastes of MSG and NMDA but they had difficulty discriminating between the tastes of aspartic acid and MSG. Rats could also easily distinguish between 10-100 mM MSG and 0.01-5 mM L-AP4. However, in two separate experiments error rates increased significantly when L-AP4 concentrations were between 10-100 mM, indicating that the tastes of L-AP4 and MSG were similar at these concentrations.

Amiloride↗
PubMed1998

Taste in chimpanzees. III: Labeled-line coding in sweet taste.

In peripheral taste the coding mechanism remains an enigma. Among coding theories the "across-fiber pattern" argues that activity across fibers codes for taste, whereas the "labeled line" claims that activity in a particular set of fibers underlies a taste quality. We showed previously that chimpanzee chorda tympani taste fibers grouped according to human taste qualities into an S-cluster, responding predominantly to sweet stimuli, a Q-cluster, sensitive to bitter tastants, and an N-cluster, stimulated by salts. The analysis showed that information in the S-line suffices to distinguish stimuli of one taste quality from the others. However, one condition for the labeled line remained: that blockage of activity in a particular line must cause blockage of one taste quality, but of no other, or its onset give rise to the sensation of a taste quality. Here we studied this requirement with gymnemic acids and miraculin. In humans and chimpanzees, gymnemic acids suppress the sweet taste of all sweeteners whereas miraculin adds a sweet taste quality to sour stimuli. Gymnemic acids also abolish miraculin-induced sweet taste. We found that gymnemic acids practically abolished the response to every sweetener in the chimpanzee S-cluster. Equally important, they had no effect on the responses of the Q- and N-clusters. After miraculin, the S-cluster fibers responded to acids as well as to sweeteners, although they had not responded to acids before miraculin. Gymnemic acids abolished this miraculin-induced response to acids and responses to sweeteners in the S-fibers. These results link the sweet taste quality to activity in fibers of the S-cluster. Thus the S-cluster fibers satisfy the definition of the labeled-line theory: "that activity in a particular fiber type represents a specific taste quality."

Animals↗
PubMed1999

The effects of beta-bungarotoxin on the morphogenesis of taste papillae and taste buds in the mouse.

Although it has been long accepted that innervation by a taste nerve is essential for maintenance of taste buds, it is not clear what role, if any, innervation plays in the morphogenesis of taste papillae and taste bud development. The following study was undertaken to determine what effects lack of sensory innervation have on the development of taste papillae and the formation of taste buds in the mouse. Timed-pregnant female mice (n = 3) at gestational day 12 (gd12) were anesthetized and a 1 microl solution (1 microg/microl) of beta-bungarotoxin (beta-BTX), a neurotoxin that disrupts sensory and motor neuron development, was injected into the amniotic cavity of two embryos per dam. Two shams were injected with PBS. Fetuses were harvested at gd18, 1 day before birth, and four beta-BTX-injected embryos, two shams and two controls were fixed in buffered paraformaldehyde. Serial sections were examined for the presence and morphology of taste papillae and taste buds. No nerve profiles were observed in beta-BTX-injected tongues. Although circumvallate papillae were present on beta-BTX tongues, only five fungiform papillae could be identified. Taste buds were present on a large percentage of fungiform papillae profiles (24%) and on circumvallate papillae in sham and control fetuses; in contrast, no taste buds were associated with taste papillae in beta-BTX fetuses. These results implicate a significant role for innervation in taste papillae and taste bud morphogenesis.

Animals↗
PubMed2004

Monosodium glutamate and sweet taste: discrimination between the tastes of sweet stimuli and glutamate in rats.

Generalization of a conditioned taste aversion (CTA) is based on similarities in taste qualities shared by the aversive substance and another taste substance. CTA experiments with rats have found that an aversion to a variety of sweet stimuli will cross-generalize with monosodium glutamate (MSG) when amiloride, a sodium channel blocker, is added to all solutions to reduce the taste of sodium. These findings suggest that the glutamate anion elicits a sweet taste sensation in rats. CTA experiments, however, generally do not indicate whether two substances have different taste qualities. In this study, discrimination methods in which rats focused on perceptual differences were used to determine if they could distinguish between the tastes of MSG and four sweet substances. As expected, rats readily discriminated between two natural sugars (sucrose, glucose) and two artificial sweeteners (saccharin, SC45647). Rats also easily discriminated between MSG and glucose, saccharin and, to a lesser extent, SC45647 when the taste of the sodium ion of MSG was reduced by the addition of amiloride to all solutions, or the addition of amiloride to all solutions and NaCl to each sweet stimulus to match the concentration of Na+ in the MSG solutions. In contrast, reducing the cue function of the Na+ ion significantly decreased their ability to discriminate between sucrose and MSG. These results suggest that the sweet qualities of glutamate taste is not as dominate a component of glutamate taste as CTA experiments suggest and these qualities are most closely related to the taste qualities of sucrose. The findings of this study, in conjunction with other research, suggest that sweet and umami afferent signaling may converge through a taste receptor with a high affinity for glutamate and sucrose or a downstream transduction mechanism. These data also suggest that rats do not necessarily perceive the tastes of these sweet stimuli as similar and that these sweet stimuli are detected by multiple sweet receptors.

Animals↗
PubMed1990

Variations in human taste bud density and taste intensity perception.

Some variations in human taste sensitivity may be due to different numbers of taste buds among subjects. Taste pores were counted on the tongue tips of 16 people with videomicroscopy, and the subjects were divided into two groups (N = 8) by the rank order of their taste bud densities. The "higher" density group averaged 374 +/- 134 taste pores/cm2, while the "lower" density group averaged 135 +/- 43 tp/cm2. The higher density group had an average fungiform papilla density which was 1.8 times greater than the lower density group and an average of 1.5 times more taste pores/papilla. The subjects also rated the intensity for 4 suprathreshold concentrations of 5 taste stimuli placed on the same region of the tongue where taste pores were counted. The group with higher taste bud densities gave significantly higher average intensity ratings for sucrose (196%), NaCl (135%) and PROP (142%), but not for citric acid (118%) and quinine HCl (110%) than the lower density group. Thus, the subjects with higher fungiform taste bud densities also reported some tastes as more intense than subjects with fewer fungiform taste buds.

Arousal↗
PubMed1979

Cross-enhancement of the sour taste on single human taste papillae.

The subjective intensity of one taste quality can be increased by prior exposure of the tongue to a different taste quality stimulus. This phenomenon, called cross-enhancement, may be the result of interactions among the physiological mechanisms that code taste quality. Another possible explanation is that the water solvent of the second stimulus acquires a taste after exposure of the tongue to the first stimulus. This water taste could add to the taste of the solute in the second stimulus and result in an increase of its subjective intensity. A third possibility is that taste receptors on the tongue may be sensitized by exposure to a taste stimulus. Using a small number of highly trained subjects, we have demonstrated that sucrose can enhance the intensity of an acid taste on the single papilla. Neither water taste nor sweet taste system activation played any role in the mediation of this enhancement. Through a series of experimentally derived inferential steps, we conclude that this phenomenon depends on the removal of protons from the acid receptors. In addition, we have demonstrated in the single papilla, that suppression of the acid taste when in mixture with sucrose can occur without sweet system activity. We conclude that sugars, through their capacity to bind protons, act to reduce the availability of protons to the acid receptors.

Adult↗
PubMed2003

[Taste disorders and recovery of the taste function after middle ear surgery].

BACKGROUND: The incidence and the scale of recovery of the taste function after middle ear surgery is usually determined by the use of anamnestic data and electrogustometry. METHODS: Taste tests (regional chemical taste test, electrogustometry and subjective evaluation) were performed preoperatively, 2 to 3 weeks and 6 to 9 months after middle ear surgery. These results were evaluated by taking the scale of chorda tympani nerve (CTN) manipulation into consideration. Three groups were chosen: group 1: no or small CTN manipulation, n = 54; group 2: strong CTN manipulation, n = 14; group 3: severed CTN, n = 50. PATIENTS: In a prospective study 118 patients were examined after middle ear surgery in the ENT-Department of the University of Rostock between 2001 and 2002. 61 females and 57 males, age from 7 - 81 years, were included. RESULTS: Complaints were observed in all three groups, mainly in groups 2 and 3. These included taste disorders, taste phenomenon and numbness of the tongue. Using regional chemical taste tests, the taste loss of group 3 could be proven for those patients with complaints in 64 % and for those patients without complaints in 27 %. The electrogustometry is more sensitive than chemical taste test. All patients had pathological thresholds after chorda cutting (78 % no thresholds; 22 % elevated thresholds). 68 out of 118 patients (58 %) had a second follow-up after 6 to 9 months after middle ear surgery. The complaints are declining in all groups. In groups 2 and 3 a recovery of taste function could be observed. Even if the number of patients with severed chorda, who suffer from taste disorders, diminishes, a recovery of the taste function could only be observed in 30 %. CONCLUSIONS: The scale of chorda manipulation is important for the recovery of the taste function after middle ear surgery. The CTN should be preserved intraoperatively, especially when an operation of the contralateral ear is planned as well.

Adolescent↗
PubMed1983

Chronic impairment of axonal transport eliminates taste responses and taste buds.

A Silastic nerve cuff containing colchicine (1% w/v) was placed around the combined lingualchorda tympani nerve of the Mongolian gerbil (Meriones unguiculatus) to evaluate the role of axonal transport in the maintenance of taste buds. After 3 days the summated gustatory impulse discharges recorded from the chorda tympani nerve were reduced by 60%, while compound action potentials had not changed appreciably. The lingual-chorda tympani nerve underwent ultrastructural changes including a loss of microtubules, an increased prominence and disorientation of neurofilaments, and a significant shrinkage in the cross-sectional area of axoplasm. The shrinkage of axoplasm and the accumulation of mitochondria and cholinesterase at the nerve cuff provided evidence that the colchicine treatment acted to impair axonal transport. More substantial pathological changes were evident in nerve ultrastructure by 15 days when both the ipsilateral chorda tympani taste responses and fungiform taste buds were nearly absent. Control cuffs lacking colchicine had little effect on chorda tympani taste responses, taste buds, or nerve ultrastructure. Eight or 15 days of nerve exposure to lumicolchicine, an isomer of colchicine with low affinity for tubulin, had no significant effect on taste responses. [3H]Colchicine was used in the nerve cuff to demonstrate that colchicine must have acted directly upon the nerve trunk, rather than the taste buds, to cause the loss of taste responses and taste buds. [3H]Colchicine levels were equal in the two sides of the tongue, whereas both the functional and structural deterioration of the taste buds were restricted to the ipsilateral side. We conclude that the loss of taste responses and taste buds was caused by chronically impaired axonal transport in gustatory axons.

Animals↗
PubMed1998

Biology of taste buds and the clinical problem of taste loss.

Taste buds are the anatomical structures that mediate the sense of taste. They comprise taste cells and nerve fibers within specialized epithelial structures. Taste cells are traditionally described by histologic methods as basal, dark, intermediate, and light cells, with the nerve fibers surrounding and infiltrating the taste buds. By means of immunohistochemical methods, taste cells and gustatory nerve fibers can be classified in functional groups based on the expression of various cell adhesion molecules and other proteins. When taste buds become damaged, the loss of the ability to taste results. This loss is not uncommon and can impact health and quality of life. Patients who receive radiation therapy for head and neck cancer often experience taste loss, which leads to compromised nutritional intake and a worse outcome than patients who do not experience taste loss. The mode of radiation damage to taste cells and nerve fibers has been investigated using cell adhesion molecules, synaptic vesicle proteins, and other cell markers. The light and intermediate cells are preferentially affected by ionizing radiation, whereas the nerve fibers remain structurally intact. Experimental studies of radiation-induced taste loss are performed via a unique animal/human model.

Ageusia↗
PubMed1996

Whole-cell recording from non-dissociated taste cells in mouse taste bud.

A method for the whole-cell recording from non-dissociated taste cells within mouse taste bud is described. The lingual epithelial sheet containing the taste buds was peeled free from the tongue by injecting a proteolytic enzyme, elastase, under the lingual epithelium and by incubating it in normal Tyrode solution at 30 degrees C. The preparation consisting of a taste bud and a small piece of the lingual epithelium was obtained by further the incubation in divalent cation-free Tyrode solution. After holding the small piece of the epithelium by a holding pipette loaded with continuous negative pressure for keeping the orientation of the taste bud, whole-cell configuration was established in a non-dissociated taste cell within the taste bud with a patch pipette containing Lucifer Yellow. Taste stimuli or blockers were applied from the third pipette placed near the taste pore under the continuous flow of bathing solution. Under this condition, we could simultaneously accomplish patch-clamping, visualization of taste cell morphology, localized taste stimulation and maintenance of microenvironment around the taste organ. Rapid responses to a relatively high concentration of salt stimuli were also obtained.

Amiloride↗
PubMed2006

Mouse taste cells with G protein-coupled taste receptors lack voltage-gated calcium channels and SNAP-25.

BACKGROUND: Taste receptor cells are responsible for transducing chemical stimuli from the environment and relaying information to the nervous system. Bitter, sweet and umami stimuli utilize G-protein coupled receptors which activate the phospholipase C (PLC) signaling pathway in Type II taste cells. However, it is not known how these cells communicate with the nervous system. Previous studies have shown that the subset of taste cells that expresses the T2R bitter receptors lack voltage-gated Ca2+ channels, which are normally required for synaptic transmission at conventional synapses. Here we use two lines of transgenic mice expressing green fluorescent protein (GFP) from two taste-specific promoters to examine Ca2+ signaling in subsets of Type II cells: T1R3-GFP mice were used to identify sweet- and umami-sensitive taste cells, while TRPM5-GFP mice were used to identify all cells that utilize the PLC signaling pathway for transduction. Voltage-gated Ca2+ currents were assessed with Ca2+ imaging and whole cell recording, while immunocytochemistry was used to detect expression of SNAP-25, a presynaptic SNARE protein that is associated with conventional synapses in taste cells. RESULTS: Depolarization with high K+ resulted in an increase in intracellular Ca2+ in a small subset of non-GFP labeled cells of both transgenic mouse lines. In contrast, no depolarization-evoked Ca2+ responses were observed in GFP-expressing taste cells of either genotype, but GFP-labeled cells responded to the PLC activator m-3M3FBS, suggesting that these cells were viable. Whole cell recording indicated that the GFP-labeled cells of both genotypes had small voltage-dependent Na+ and K+ currents, but no evidence of Ca2+ currents. A subset of non-GFP labeled taste cells exhibited large voltage-dependent Na+ and K+ currents and a high threshold voltage-gated Ca2+ current. Immunocytochemistry indicated that SNAP-25 was expressed in a separate population of taste cells from those expressing T1R3 or TRPM5. These data indicate that G protein-coupled taste receptors and conventional synaptic signaling mechanisms are expressed in separate populations of taste cells. CONCLUSION: The taste receptor cells responsible for the transduction of bitter, sweet, and umami stimuli are unlikely to communicate with nerve fibers by using conventional chemical synapses.

Animals↗
PubMed2003

Taste avoidance and taste aversion: evidence for two different processes.

The terms conditioned taste avoidance and conditioned taste aversion are often used interchangeably in the literature; however, considerable evidence indicates that they may represent different processes. Conditioned taste avoidance is measured by the amount that a rat consumes in a consumption test that includes both appetitive phases and consummatory phases of responding. However, conditioned taste aversion is more directly assessed with the taste reactivity test, which includes only the consummatory phase of responding. Rats display a conditioned taste aversion as conditioned rejection reactions (gapes, chin rubs, and paw treads) during an intraoral infusion of a nausea-paired flavored solution. Treatments that produce nausea are not necessary for the establishment of taste avoidance, but they are necessary for the establishment of taste aversion. Furthermore, treatments that alleviate nausea modulate neither the establishment nor the expression of taste avoidance, but they interfere with both the establishment and the expression of taste aversion. Considerable evidence exists indicating that these two measures are independent of one another. Taste avoidance may be motivated by conditioned fear rather than conditioned nausea, but taste aversion (as reflected by rejection reactions) may be motivated by conditioned nausea.

Animals↗