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At least 1,009 records · Page 56Linked to original sources
PubMed1996

Measurement of membrane potential and [Ca2+]i in cell ensembles: application to the study of glutamate taste in mice.

We have studied the spectral properties of the voltage-sensitive dye, 1-(3-sulfonatopropyl)-4-[beta [2-(di-n-octylamino)-6-naphtyl]vinyl] pyridinium betaine (di-8-ANEPPS), and the Ca(2+)-sensitive dye, fura-2, in azolectin liposomes and in isolated taste buds from mouse. We find that the fluorescence excitation spectra of di-8-ANEPPS and fura-2 are largely nonoverlapping, allowing alternate ratio measurements of membrane potential and intracellular calcium ([Ca2+]i). There is a small spillover of di-8-ANEPPS fluorescence at the excitation wavelengths used for fura-2 (340 and 360 nm). However, voltage-induced changes in the fluorescence of di-8-ANEPPS, excited at the fura-2 wavelengths, are small. In addition, di-8-ANEPPS fluorescence is localized to the membrane, whereas fura-2 fluorescence is distributed throughout the cytoplasm. Because of this, the effect of spillover of di-8-ANEPPS fluorescence in the [Ca2+]i estimate is < 1%, under the appropriate conditions. We have applied this method to study of the responses of multiple taste cells within isolated taste buds. We show that membrane potential and [Ca2+]i can be measured alternately in isolated taste buds from mouse. Stimulation with glutamate and glutamate analogs indicates that taste cells express both metabotropic and ionotropic receptors. The data suggest that the receptors responding to 2-amino-4-phosphonobutyrate (L-AP4), presumably metabotropic L-glutamate receptors, do not mediate excitatory glutamate taste responses.

Animals↗
PubMedDate not supplied

Experience-induced changes in taste identification of monosodium glutamate.

Taste sensitivity for a given subject generally has been thought to be genetically determined and not plastic. Yet experience-inducible changes in human taste and olfactory sensitivities have been reported. To test a taste induction hypothesis, we exposed 17 Americans/Europeans to monosodium glutamate (MSG) in food and then compared their ability to identify MSG taste with that of 2 control groups (18 Americans/Europeans without MSG exposure and 18 Japanese). When tested on Day 11 or 12, the Americans/Europeans exposed to MSG were able to identify MSG at significantly lower concentrations than the Americans/Europeans without MSG exposure. Moreover, Japanese subjects who had prior extensive experience with MSG in Japanese food were able to identify MSG at significantly lower concentrations than the two American/European groups. The differences in identification ability between the two American/European groups challenge the notion of taste sensitivity as stable over time and support the hypothesis of an experience-inducible component in human taste.

Adult↗
PubMed1999

Effect of medications on taste: example of amitriptyline HCl.

Use of medications is a major factor that contributes to taste losses in the elderly. Epidemiological studies suggest that community-dwelling elderly over the age of 65 use an average of 2.9 to 3.7 medications, and this number increases significantly for elderly living in retirement and nursing homes. The tricyclic antidepressant amitriptyline HCl is used by at least half a million people aged 65 years or more. In human studies performed here, amitriptyline HCl was found to have a bitter, unpleasant taste of its own. In addition, it blocked responses to other taste stimuli in both humans and gerbils. This blockage in humans was greater when amitriptyline HCl was applied continuously to the tongue than when it was applied intermittently. Continuous application of the drug affected all of the taste qualities to varying degrees, while intermittent application led to taste decrements only for salts. Electrophysiological studies in gerbils also revealed taste decrements after a short adaptation to amitriptyline HCl.

Adaptation, Physiological↗
PubMed2003

The receptors for mammalian sweet and umami taste.

Sweet and umami (the taste of monosodium glutamate) are the main attractive taste modalities in humans. T1Rs are candidate mammalian taste receptors that combine to assemble two heteromeric G-protein-coupled receptor complexes: T1R1+3, an umami sensor, and T1R2+3, a sweet receptor. We now report the behavioral and physiological characterization of T1R1, T1R2, and T1R3 knockout mice. We demonstrate that sweet and umami taste are strictly dependent on T1R-receptors, and show that selective elimination of T1R-subunits differentially abolishes detection and perception of these two taste modalities. To examine the basis of sweet tastant recognition and coding, we engineered animals expressing either the human T1R2-receptor (hT1R2), or a modified opioid-receptor (RASSL) in sweet cells. Expression of hT1R2 in mice generates animals with humanized sweet taste preferences, while expression of RASSL drives strong attraction to a synthetic opiate, demonstrating that sweet cells trigger dedicated behavioral outputs, but their tastant selectivity is determined by the nature of the receptors.

Animals↗
PubMed2002

[Taste disorders].

PURPOSE: This review focuses on the present state of the question about taste disorders with reference to their associated factors, diagnostic methods, and potential effects. CURRENT KNOWLEDGE AND KEY POINTS: Taste disorders may be induced by many drugs and are associated to a number of acute or chronic diseases. Patients may be asked about their taste complaints, and taste thresholds may be determined by electrogustometry or chemical gustometry. Taste impairment may provide a good indicator to the course of some diseases such as diabetes mellitus in which hypogeusia predicts occurrence of degenerative complications. Dysgeusia may induce nutritional disorders and contribute to wasting in chronic liver disease, cancer, or human immunodeficiency virus infected patients. Mechanisms involved in dysgeusia are more than one in a patient. Taste disturbance may be secondary to a variety of causes that include zinc deficiency, lesions of the lingual epithelium, neurological impairment, and a pharmacological effect. FUTURE PROSPECTS AND PROJECTS: A better understanding of the transduction mechanisms of the gustatory signal and the main pathogenic factors involved in dysgeusia may possibly improve the follow-up of the concerned patients notably in terms of nutritional status.

Acute Disease↗
PubMed1999

Taste and food preferences as predictors of dietary practices in young women.

OBJECTIVE: To investigate links between taste responses, self-reported food preferences and selected dietary outcomes in young women. METHODS: Subjects were 159 women, with a mean age of 27.0 years. Taste responses were measured using aqueous solutions of 6-n-propylthiouracil (PROP) and sucrose. All subjects completed a 171-item food preference checklist, using nine-point category scales. Food preference data were reduced using principal components factor analyses, with the internal consistency of factor-based subscales established using Cronbach's alpha. Dietary intakes, available for a subset of 87 women, were based on 3 days of food records. Estimated intakes of carbohydrate, fibre and beta-carotene were the key dietary outcome variables. RESULTS: Genetically-mediated sensitivity to the bitter taste of PROP was associated with reduced preferences for Brussels sprouts, cabbage, spinach and coffee beverages. Higher preferences for sucrose in water were associated with increased preferences for sweet desserts. Food preferences, in turn, were associated with measures of current diet. Reduced acceptability of vegetables and fruits was associated with lower estimated intakes of carbohydrate, fibre and beta-carotene. CONCLUSIONS: Taste responses to sucrose and PROP were predictive of some food preferences. Food preferences, in turn, were associated with food consumption patterns. Given that taste responsiveness to PROP is an inherited trait, there may be further links between genetic taste markers, eating habits and the selection of healthful diets.

Adult↗
PubMed2000

A family of candidate taste receptors in human and mouse.

The gustatory system of mammals can sense four basic taste qualities, bitter, sweet, salty and sour, as well as umami, the taste of glutamate. Previous studies suggested that the detection of bitter and sweet tastants by taste receptor cells in the mouth is likely to involve G-protein-coupled receptors. Although two putative G-protein-coupled bitter/sweet taste receptors have been identified, the chemical diversity of bitter and sweet compounds leads one to expect that there is a larger number of different receptors. Here we report the identification of a family of candidate taste receptors (the TRBs) that are members of the G-protein-coupled receptor superfamily and that are specifically expressed by taste receptor cells. A cluster of genes encoding human TRBs is located adjacent to a Prp gene locus, which in mouse is tightly linked to the SOA genetic locus that is involved in detecting the bitter compound sucrose octaacetate. Another TRB gene is found on a human contig assigned to chromosome 5p15, the location of a genetic locus (PROP) that controls the detection of the bitter compound 6-n-propyl-2-thiouracil in humans.

Amino Acid Sequence↗
PubMed2002

An amino-acid taste receptor.

The sense of taste provides animals with valuable information about the nature and quality of food. Mammals can recognize and respond to a diverse repertoire of chemical entities, including sugars, salts, acids and a wide range of toxic substances. Several amino acids taste sweet or delicious (umami) to humans, and are attractive to rodents and other animals. This is noteworthy because L-amino acids function as the building blocks of proteins, as biosynthetic precursors of many biologically relevant small molecules, and as metabolic fuel. Thus, having a taste pathway dedicated to their detection probably had significant evolutionary implications. Here we identify and characterize a mammalian amino-acid taste receptor. This receptor, T1R1+3, is a heteromer of the taste-specific T1R1 and T1R3 G-protein-coupled receptors. We demonstrate that T1R1 and T1R3 combine to function as a broadly tuned L-amino-acid sensor responding to most of the 20 standard amino acids, but not to their D-enantiomers or other compounds. We also show that sequence differences in T1R receptors within and between species (human and mouse) can significantly influence the selectivity and specificity of taste responses.

Alleles↗
PubMed2002

A transient receptor potential channel expressed in taste receptor cells.

We used differential screening of cDNAs from individual taste receptor cells to identify candidate taste transduction elements in mice. Among the differentially expressed clones, one encoded Trpm5, a member of the mammalian family of transient receptor potential (TRP) channels. We found Trpm5 to be expressed in a restricted manner, with particularly high levels in taste tissue. In taste cells, Trpm5 was coexpressed with taste-signaling molecules such as alpha-gustducin, Ggamma13, phospholipase C-beta2 (PLC-beta2) and inositol 1,4,5-trisphosphate receptor type III (IP3R3). Our heterologous expression studies of Trpm5 indicate that it functions as a cationic channel that is gated when internal calcium stores are depleted. Trpm5 may be responsible for capacitative calcium entry in taste receptor cells that respond to bitter and/or sweet compounds.

Animals↗
PubMed2005

Ethanol modulates the VR-1 variant amiloride-insensitive salt taste receptor. II. Effect on chorda tympani salt responses.

The effect of ethanol on the amiloride- and benzamil (Bz)-insensitive salt taste receptor was investigated by direct measurement of intracellular Na(+) activity ([Na(+)](i)) using fluorescence imaging in polarized fungiform taste receptor cells (TRCs) and by chorda tympani (CT) taste nerve recordings. CT responses to KCl and NaCl were recorded in Sprague-Dawley rats, and in wild-type (WT) and vanilloid receptor-1 (VR-1) knockout mice (KO). CT responses were monitored in the presence of Bz, a specific blocker of the epithelial Na(+) channel (ENaC). CT responses were also recorded in the presence of agonists (resiniferatoxin and elevated temperature) and antagonists (capsazepine and SB-366791) of VR-1 that similarly modulate the Bz-insensitive VR-1 variant salt taste receptor. In the absence of mineral salts, ethanol induced a transient decrease in TRC volume and elicited only transient phasic CT responses. In the presence of mineral salts, ethanol increased the apical cation flux in TRCs without a change in volume, increased transepithelial electrical resistance across the tongue, and elicited CT responses that were similar to salt responses, consisting of both a phasic component and a sustained tonic component. At concentrations <50%, ethanol enhanced responses to KCl and NaCl, while at ethanol concentrations >50%, those CT responses were inhibited. Resiniferatoxin and elevated temperature increased the sensitivity of the CT response to ethanol in salt-containing media, and SB-366791 inhibited the effect of ethanol, resiniferatoxin, and elevated temperature on the CT responses to mineral salts. VR-1 KO mice demonstrated no Bz-insensitive CT response to NaCl and no sensitivity to ethanol. We conclude that ethanol increases salt taste sensitivity by its direct action on the Bz-insensitive VR-1 variant salt taste receptor.

Algorithms↗
PubMed1996

Are the tastes of polycose and monosodium glutamate unique?

To study whether Polycose and monosodium L-glutamate (L-MSG) have unique tastes differing from the traditional four basic tastes, chemosensory profiles were established for Polycose, L-MSG and a group of related compounds (sucrose, maltose, monosodium D-glutamate (D-MSG), sodium chloride, calcium chloride). Flavors were assessed using whole-mouth tests in human subjects with nose open or clamped to reduce olfactory input. Polycose (a mixture of glucose-based oligosaccharides) had a flavor consisting of an olfactory component and a maltose-like taste. L-MSG and D-MSG profiles differed from each other, and from NaCl and CaCl2. L-MSG had a lower threshold and a higher frequency of 'other' tastes than the D form. The data do not support a 'polysaccharide' taste, but suggest a chiral receptor site for 'umami' taste.

Adult↗
PubMed1996

Phagocytic cells in the taste buds of rat circumvallate papillae after denervation.

Phagocytic cells in the taste buds of rat circumvallate papillae after the sectioning of bilateral glossopharyngeal nerves were examined by electron microscopy and immunohistochemistry. Electron micrographs taken 1 day after denervation revealed that flat-shaped cells were present just beneath the taste buds and that their cellular processes extended toward the debris from the degenerating taste buds. At 2-6 days after denervation, long and thin processes of the flat cells surrounded the debris and appeared to have taken them up into the cytoplasm as small vesicles. Evidence for phagocytosis by the flat cells was seen up to 9 days after denervation and again at 24 and 40 days, in correlation to the degeneration and regeneration of the taste buds. Pre-embedding immunohistochemistry using anti-vimentin antibody showed that flat cells strongly reacted with vimentin. Light microscopic immunohistochemistry using anti-macrophage antibodies (ED1, ED2) showed that throughout the post-operative days macrophages were not present underneath or within the taste buds. Most of the ED2-immunoreactive resident macrophages were located in the deep layer of connective tissue, and a few were found in the nerve bundle. ED1-immunoreactive cells were seen in the duct cells of von Ebner's glands and a few were in the trench wall of circumvallate papillae; however, they were also immunoreactive for anti-OX62 antibody, which recognizes dendritic cells. The results indicate that the phagocytic cells of the taste buds are fibroblasts, not macrophages. Moreover, resident macrophages participate in phagocytosis of degenerated nerves together with Schwann cells.

Animals↗
PubMed1998

Effects of chorda tympani nerve anesthesia on taste responses in the NST.

Human clinical and psychophysical observations suggest that the taste system is able to compensate for losses in peripheral nerve input, since patients do not commonly report decrements in whole mouth taste following chorda tympani nerve damage or anesthesia. Indeed, neurophysiological data from the rat nucleus of the solitary tract (NST) suggests that a release of inhibition (disinhibition) may occur centrally following chorda tympani nerve anesthesia. Our purpose was to study this possibility further. We recorded from 59 multi- and single-unit taste-responsive sites in the rat NST before, during and after recovery from chorda tympani nerve anesthesia. During anesthesia, average anterior tongue responses were eliminated but no compensatory increases in palatal or posterior tongue responses were observed. However, six individual sites displayed increased taste responsiveness during anesthesia. The average increase was 32.9%. Therefore, disinhibition of taste responses was observed, but infrequently and to a small degree in the NST At a subset of sites, chorda tympani-mediated responses decreased while greater superficial petrosal-mediated responses remained the same during anesthesia. Since this effect was accompanied by a decrease in spontaneous activity, we propose that taste compensation may result in part by a change in signal-to-noise ratio at a subset of sites.

Adaptation, Physiological↗
PubMed2000

Glossopharyngeal taste responses of the channel catfish to binary mixtures of amino acids.

This study examines the neural processing of binary mixtures in the glossopharyngeal (IX) taste system of the channel catfish, Ictalurus punctatus, and finds that the nature of the components of a mixture determines the intensity of the neural response to it. Taste buds in fish innervated by IX are located along the gill rakers of the first gill arch and rostral floor of the oral cavity, and function primarily in the consummatory phase of feeding behavior; however, few studies of IX taste responses have been reported in any species of teleost. Here, we report IX taste responses to eight different binary mixtures of amino acids whose components were adjusted to be approximately equipotent in electrophysiological recordings. Four binary (group I) mixtures whose components were indicated from prior electrophysiological cross-adaptation experiments to bind to independent receptor sites resulted in significantly larger (22% average increase) integrated IX taste activity than four other (group II) binary mixtures whose components were indicated to bind to the same or highly cross-reactive receptor sites. These results are similar to those observed previously from facial nerve recordings in channel catfish, and to olfactory and taste responses in other vertebrate and invertebrate species. The group I results help to explain behavioral observations that chemical mixtures of chemosensory stimuli are often more stimulatory than their individual components.

Amino Acids↗
PubMed2002

Taste confusions following chlorhexidine treatment.

Chlorhexidine, a bitter bis-biguanide antiseptic, is the only known blocker of the human salty taste. In order to characterize the effects of chlorhexidine on stimulus identification, taste confusion matrix (TCM) performance was measured for subjects treated with 1.34 mM chlorhexidine gluconate (n = 9) and water controls (n = 9). Ten stimuli [water, 0.1 M NaCl, 0.1 M KCl, 0.1 mM quinine-HCl (QHCl), 0.1 M monosodium glutamate (MSG), 3 mM citric acid, 0.3 M sucrose and mixtures of NaCl, QHCl and citric acid with sucrose] were presented in 10 replicates for identification from a list of 10 stimulus names. T(10), a measure of performance consistency from information theory, was lower for chlorhexidine-treated subjects (2.02 +/- 0.11 bits) than controls (2.73 +/- 0.11 bits) (P < 0.0001). T(2), an indirect measure of pairwise stimulus discrimination, approached chance levels (0.40 bit) in chlorhexidine-treated subjects for all possible pairs of NaCl, KCl, QHCl and water, as well as pairs composed of sucrose and the NaCl-sucrose and quinine-sucrose mixtures. In controls T(2) values approached perfect scores (1.00 bit) for all stimulus pairs except NaCl-KCl and NaCl-MSG. The results demonstrate a decreased ability to identify taste stimuli that is consistent with alterations in the ability of stimuli to elicit salty and bitter taste perceptions. As a selective, effective, persistent and reversible blocker of taste perceptions, chlorhexidine should prove useful in defining taste mechanisms in humans.

Adult↗
PubMed2002

Partial rescue of taste responses of alpha-gustducin null mice by transgenic expression of alpha-transducin.

The transduction of responses to bitter and sweet compounds utilizes guanine nucleotide binding proteins (G proteins) and their coupled receptors. Alpha-gustducin, a transducin-like G protein alpha-subunit, and rod alpha-transducin are expressed in taste receptor cells. Alpha-gustducin knockout mice have profoundly diminished behavioral and electrophysiological responses to many bitter and sweet compounds, although these mice retain residual responses to these compounds. Alpha-gustducin and rod alpha-transducin are biochemically indistinguishable in their in vitro interactions with retinal phosphodiesterase, rhodopsin and G protein betagamma-subunits. To determine if alpha-transducin can function in taste receptor cells and to compare the function of alpha-gustducin versus alpha-transducin in taste transduction in vivo, we generated transgenic mice that express alpha-transducin under the control of the alpha-gustducin promoter in the alpha-gustducin null background. Immunohistochemistry showed that the alpha-transducin transgene was expressed in about two-thirds of the alpha-gustducin lineage of taste receptor cells. Two-bottle preference tests showed that transgenic expression of rod alpha-transducin partly rescued responses to denatonium benzoate, sucrose and the artificial sweetener SC45647, but not to quinine sulfate. Gustatory nerve recordings showed a partial rescue by the transgene of the response to sucrose, SC45647 and quinine, but not to denatonium. These results demonstrate that alpha-transducin can function in taste receptor cells and transduce some taste cell responses. Our results also suggest that alpha-transducin and alpha-gustducin may differ, at least in part, in their function in these cells, although this conclusion must be qualified because of the limited fidelity of the transgene expression.

Analgesics, Non-Narcotic↗
PubMed2004

Analysis of slow hyperpolarizing potentials in frog taste cells induced by glossopharyngeal nerve stimulation.

Electrical stimulation of the frog glossopharyngeal (GP) nerve evoked slow hyperpolarizing potentials (HPs) in taste cells. This study aimed to clarify whether slow HPs were postsynaptically induced in taste cells. The slow HPs were recorded intracellularly with a microelectrode. When Ca2+ concentration in the blood plasma was decreased to approximately 0.5 mM, the amplitude of slow HPs reduced and their latency lengthened. When the Ca2+ concentration was increased to approximately 20 mM, the amplitude of slow HPs increased and their latency shortened. Addition of Cd2+ to the plasma greatly reduced the amplitude of slow HPs and lengthened their latency. These data suggest that the slow HPs are dependent on presynaptic activities in the GP nerve terminals in the taste disk. Of various antagonists injected intravenously for blocking receptors of neurotransmitter biogenic amines and peptides, only antagonists for substance P blocked the slow HPs at 2-4 mg/kg body wt. Application of substance P of 2 mg/kg to the plasma induced hyperpolarizing responses in taste cells, whose amplitude was the same as that of the slow HPs induced by GP nerve stimulation. Application of a nonselective cation channel antagonist, flufenamic acid, to the plasma blocked the slow HPs. These results suggest that the slow HPs are generated by closing the nonselective cation channels in the postsynaptic membrane of taste cells following possible release of substance P from the GP nerve terminals in the taste disk.

Action Potentials↗
PubMed2006

Effect of ciguatoxin 3C on voltage-gated Na+ and K+ currents in mouse taste cells.

The marine dinoflagellate Gambierdiscus toxicus produces highly lipophilic, polycyclic ether toxins that cause a seafood poisoning called ciguatera. Ciguatoxins (CTXs) and gambierol represent the two major causative agents of ciguatera intoxication, which include taste alterations (dysgeusiae). However, information on the mode of action of ciguatera toxins in taste cells is scarce. Here, we have studied the effect of synthetic CTX3C (a CTX congener) on mouse taste cells. By using the patch-clamp technique to monitor membrane ion currents, we found that CTX3C markedly affected the operation of voltage-gated Na(+) channels but was ineffective on voltage-gated K(+) channels. This result was the exact opposite of what we obtained earlier with gambierol, which inhibits K(+) channels but not Na(+) channels. Thus, CTXs and gambierol affect with high potency the operation of separate classes of voltage-gated ion channels in taste cells. Our data suggest that taste disturbances reported in ciguatera poisoning might be due to the ability of ciguatera toxins to interfere with ion channels in taste buds.

Animals↗