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At least 451 records · Page 25Linked to original sources
PubMed2003

The effect of orthognathic surgery on taste function on the palate and tongue.

PURPOSE: Perceived taste intensity and taste quality identification on localized regions of the palate and tongue were examined for 9 patients before orthognathic surgery and again at 1 to 2 and 6 to 9 months after surgery. Taste function would be at risk on the palate after maxillary Le Fort I osteotomy (LFI) and on the tongue after mandibular sagittal split osteotomy (SSO) because of potential damage to peripheral nerves conducting afferent chemosensory information from these regions. PATIENTS AND METHODS: Three patients had LFI and SSO, 1 had LFI only, and 5 had SSO only. Patients rated taste intensity (using a 10-point fixed-interval scale) and identified taste quality of 4 solutions (NaCl, sucrose, citric acid, and quinine.HCl) brushed with a cotton-tipped applicator on each of 6 oral locations (left and right soft palate, left and right anterior and posterolateral tongue). RESULTS: Perceived taste intensity of NaCl, sucrose, and citric acid was reduced on average to 34% of presurgery values on the palate for patients who underwent LFI, but the taste intensity of quinine was not affected. LFI also affected the ability to correctly identify the quality of tastants applied to the palate: Patients made 38% correct quality identifications postsurgery compared with 91% presurgery. Perceived taste intensity of quinine.HCl placed on the tongue was reduced to 72% of its presurgery value after SSO, but the taste intensities of NaCl, sucrose, and citric acid were not affected. Correct quality identifications of sucrose, citric acid, and quinine.HCl were reduced to 75% at 2 months post-SSO compared with 96% presurgery and at 6 months postsurgery, but identification for NaCl was 96% before and after surgery. CONCLUSION: In the patients studied, taste function on the palate was significantly decreased for 6 to 9 months after LFI, likely a result of impairment of function of the greater superficial petrosal branch of the facial nerve. Lingual taste function, reduced at 1 to 2 months after SSO, likely due to impaired chorda tympani nerve function, improved by 6 to 9 months. Palatal and lingual neurosensory testing can be used to identify reversible sequelae of oral maxillofacial surgery.

Adolescent↗
PubMed2006

An analysis of 5'-inosine and 5'-guanosine monophosphate taste in rats.

Inosine monophosphate (IMP) and guanosine monophosphate (GMP) elicit an umami taste in humans and synergistically increase the intensity of the umami taste of monosodium glutamate (MSG). Conditioned taste aversion (CTA) studies in rodents indicate that these nucleotides and MSG elicit quite similar tastes, but recent physiological evidence suggests that these nucleotides and MSG may not activate the same population of taste receptors and therefore may not elicit identical taste qualities. This study reports the findings of several behavioral experiments with rats that compared the taste properties of IMP and GMP with each other and with those of MSG. Well-trained rats were able to detect both nucleotides at nanomolar concentrations, but they did not respond to either nucleotide in two-bottle preference tests or brief-access CTA tests at concentrations less than 0.5 mM. Discrimination experiments found that the tastes of these nucleotides could not be discriminated from each other, but both could be discriminated from MSG, even when the taste of Na(+) was controlled. Overall, these experiments indicate the taste properties of the two 5'-ribonucleotides are quite similar to each other, and even though they may elicit an umami sensation, these sensations are not identical to the taste of MSG.

Animals↗
PubMed2004

The mammalian amiloride-insensitive non-specific salt taste receptor is a vanilloid receptor-1 variant.

The amiloride-insensitive salt taste receptor is the predominant transducer of salt taste in some mammalian species, including humans. The physiological, pharmacological and biochemical properties of the amiloride-insensitive salt taste receptor were investigated by RT-PCR, by the measurement of unilateral apical Na+ fluxes in polarized rat fungiform taste receptor cells and by chorda tympani taste nerve recordings. The chorda tympani responses to NaCl, KCl, NH4Cl and CaCl2 were recorded in Sprague-Dawley rats, and in wild-type and vanilloid receptor-1 (VR-1) knockout mice. The chorda tympani responses to mineral salts were monitored in the presence of vanilloids (resiniferatoxin and capsaicin), VR-1 antagonists (capsazepine and SB-366791), and at elevated temperatures. The results indicate that the amiloride-insensitive salt taste receptor is a constitutively active non-selective cation channel derived from the VR-1 gene. It accounts for all of the amiloride-insensitive chorda tympani taste nerve response to Na+ salts and part of the response to K+, NH4+ and Ca2+ salts. It is activated by vanilloids and temperature (> 38 degrees C), and is inhibited by VR-1 antagonists. In the presence of vanilloids, external pH and ATP lower the temperature threshold of the channel. This allows for increased salt taste sensitivity without an increase in temperature. VR-1 knockout mice demonstrate no functional amiloride-insensitive salt taste receptor and no salt taste sensitivity to vanilloids and temperature. We conclude that the mammalian non-specific salt taste receptor is a VR-1 variant.

Amiloride↗
PubMed2005

Human taste genetics.

Humans show substantial differences in taste sensitivity to many different substances. Some of this variation is known to be genetic in origin, and many other inter-individual differences are likely to be partially or wholly determined by genetic mechanisms. Recent advances in the understanding of taste at the molecular level have provided candidate genes that can be evaluated for contributions to phenotypic differences in taste abilities. This approach has provided an understanding of variation in the ability to taste phenylthiocarbamide (PTC), and has resolved long-standing controversies about the genetics of this classic human genetic trait. Significant coding sequence variation exists in taste receptor genes, which suggests that PTC tasting may indicate more general taste sensory variation. However, many aspects of taste perception remain poorly characterized. Better understanding of the molecular components of salty and sour tastes is still needed, as is a more complete picture of second messenger and downstream signaling mechanisms for all taste modalities. More general studies of linkage and association between genetic markers and taste phenotypes may reveal genes encoding proteins that were previously unsuspected to be involved in this sensory process.

Evolution, Molecular↗
PubMed2001

Mouse taste cells with glialike membrane properties.

Taste buds are sensory structures made up by tightly packed, specialized epithelial cells called taste cells. Taste cells are functionally heterogeneous, and a large proportion of them fire action potentials during chemotransduction. In view of the narrow intercellular spaces within the taste bud, it is expected that the ionic composition of the extracellular fluid surrounding taste cells may be altered significantly by activity. This consideration has led to postulate the existence of glialike cells that could control the microenvironment in taste buds. However, the functional identification of such cells has been so far elusive. By using the patch-clamp technique in voltage-clamp conditions, I identified a new type of cells in the taste buds of the mouse vallate papilla. These cells represented about 30% of cells patched in taste buds and were characterized by a large leakage current. Accordingly, I named them "Leaky" cells. The leakage current was carried by K(+), and was blocked by Ba(2+) but not by tetraethylammonium (TEA). Other taste cells, such as those possessing voltage-gated Na(+) currents and thought to be chemosensory in function, did not express any sizeable leakage current. Consistent with the presence of a leakage conductance, Leaky cells had a low input resistance (approximately 0.25 G Omega). In addition, their zero-current ("resting") potential was close to the equilibrium potential for potassium ions. The electrophysiological analysis of the membrane currents remaining after pharmacological block by Ba(2+) revealed that Leaky cells also possessed a Cl(-) conductance. However, in resting conditions the membrane of these cells was about 60 times more permeable to K(+) than to Cl(-). The resting potassium conductance in Leaky cells could be involved in dissipating rapidly the increase in extracellular K(+) during action potential discharge in chemosensory cells. Thus Leaky cells might represent glialike elements in taste buds. These findings support a model in which specific cells control the chemical composition of intercellular fluid in taste buds.

Animals↗
PubMed2004

Taste buds: development and evolution.

The gustatory system in vertebrates comprises peripheral receptors (taste buds), innervated by three cranial nerves (VII, IX, and X), and a series of central neural centers and pathways. All vertebrates, with the exception of hagfishes, have taste buds. These receptors vary morphologically in different vertebrates but usually consist of at least four types of cells (dark, light, basal, and stem cells). An out-group analysis indicates that taste buds were restricted to the oropharynx, primitively, and that external taste buds, distributed over the head and, in some cases, even the trunk, evolved a number of times independently. The sensory neurons of the cranial nerves that innervate taste buds are believed to arise from epibranchial placodes, which are induced by pharyngeal endoderm, but it has never been demonstrated experimentally that these sensory neurons do, in fact, arise from these placodes. Although many details of the development of the innervation of taste buds are still unknown, it is now clear that taste buds are induced from either ecto- or endodermal epithelia, rather than arising from either placodes or neural crest. At present, there are two developmental models of taste bud induction: The neural induction model claims that peripheral nerve fibers induce taste buds, whereas the early specification model claims that oropharyngeal epithelium is specified by or during gastrulation and that taste buds arise from cell-cell interactions within the specified epithelium. There is now substantial evidence that the early specification model best describes the induction of taste buds.

Animals↗
PubMed2003

Leptin modulates behavioral responses to sweet substances by influencing peripheral taste structures.

Leptin is a hormone that regulates body weight homeostasis mainly via the hypothalamic functional leptin receptor Ob-Rb. Recently, we proposed that the taste organ is a new peripheral target for leptin. Leptin selectively inhibits mouse taste cell responses to sweet substances and thereby may act as a sweet taste modulator. The present study further investigated leptin action on the taste system by examining expression of Ob-Rb in taste cells and behavioral responses to sweet substances in leptin-deficient ob/ob, and Ob-Rb-deficient db/db mice and their normal litter mates. RT-PCR analysis showed that Ob-Rb was expressed in taste cells in all strains tested. The db/db mice, however, had a RT-PCR product containing an abnormal db insertion that leads to an impaired shorter intracellular domain. In situ hybridization analysis showed that the hybridization signals for normal Ob-Rb mRNA were detected in taste cells in lean and ob/ob mice but not in db/db mice. Two different behavioral tests, one using sweet-bitter mixtures as taste stimuli and the other a conditioned taste aversion paradigm, demonstrated that responses to sucrose and saccharin were significantly decreased after ip injection of leptin in ob/ob and normal littermates, but not in db/db mice. These results suggest that leptin suppresses behavioral responses to sweet substances through its action on Ob-Rb in taste cells. Such taste modulation by leptin may be involved in regulation for food intake.

Animals↗
PubMed1989

[Taste].

Taste has a dual role. Like other senses it informs the individual about the external world, but unlike other senses it connects that perception with information about the internal environment. The principal function of taste is similar in all higher species. Molecules act on specialized sensory cells (= taste cells) in various regions of the oral cavity thus triggering signals, which are relayed to the cortex via afferent nerves, the caudal hindbrain and the thalamus. Taste afferents also reach the hypothalamus and the limbic system. The taste of food triggers physiological and behavioral reactions in man and animals. Stimulation of taste cells immediately elicits salivation, secretion of gastric acid and pancreatic juice as well as secretion of gastrointestinal and pancreatic hormones. Innate and learned taste preferences or aversions play an important role in food selection and taste aversions are considered to be reliable indicators of malaise. Neural signals from the periphery or humoral factors which are sensed by receptors in the central nervous system both can change the acceptance of a certain taste. Endogenous opiates in the brain seem to play a special role in the modulation of taste perception. The amygdala is apparently a brain area which is particularly important for taste perception.

Animals↗
PubMedDate not supplied

Clinical evaluation of taste.

Partial loss of taste function can take a variety of forms. Losses can be specific to one taste quality or to one tongue locus. In addition, the shapes of psychophysical functions can be altered so that taste intensity no longer grows normally with concentration. Magnitude matching, an efficient psychophysical scaling method (based on magnitude estimation of stimuli from two sensory continua), can provide a relatively quick assessment of a patient's ability to taste the four taste qualities--sweet, salty, sour, and bitter. When taste intensity and loudness are scaled in the same session, a person with normal hearing who has taste loss will match taste intensities to abnormally weak sounds. Spatial losses are detected by placing pieces of filter paper soaked in taste solutions on specific tongue loci. Dysgeusia, the presence of a chronic taste in the mouth, can result from abnormal substances in the mouth (e.g., via saliva or from poor oral hygiene) or can reflect disorders of the central nervous system.

Humans↗
PubMed2004

Genetics of human taste perception.

Genetic approaches are rapidly yielding new information about our sense of taste. This information comes from both molecular studies of genes encoding taste receptors and other taste-signaling components, and from studies of inherited variation in taste abilities. Our understanding of bitter taste has advanced by combined information from discovery and study of the TAS2R family of taste receptor genes, hand in hand with genetic linkage and positional cloning studies, notably on the ability to taste phenylthiocarbamide (PTC). Sweet and umami tastes, mediated by TAS1R receptors, are becoming well-characterized at the molecular genetic level, and these taste classes are now targets for linkage, positional cloning, and genetic association strategies. Salty and sour tastes are still poorly characterized in genetic terms, and represent opportunities for the future.

Animals↗
PubMed1996

Differential localization of putative amino acid receptors in taste buds of the channel catfish, Ictalurus punctatus.

The taste system of catfish, having distinct taste receptor sites for L-alanine and L-arginine, is highly sensitive to amino acids. A previously described monoclonal antibody (G-10), which inhibits L-alanine binding to a partial membrane fraction (P2) derived from catfish (Ictalurus punctatus) taste epithelium, was found in Western blots to recognize a single band, at apparent MW of 113,000 D. This MW differs from the apparent MW for the presumed arginine receptor identified previously by PHA-E lectin affinity. In order to test whether PHA-E lectin actually reacts with the arginine-receptor, reconstituted membrane proteins partially purified by PHA-E affinity were used in artificial lipid bilayers. These reconstituted channels exhibited L-arginine-activated activity similar to that found in taste cell membranes. Accordingly, we utilized the PHA-E lectin and G-10 antibody as probes to differentially localize the L-alanine and L-arginine binding sites on the apical surface of catfish taste buds. Each probe labels numerous, small (0.5-1.0 micron) patches within the taste pore of each taste bud. This observation suggests that each bud is not tuned to a single taste substance, but contains putative receptor sites for both L-arginine and L-alanine. Further, analysis of double-labeled tissue reveals that the PHA-E and G-10 sites tend to be separate within each taste pore. These findings imply that in catfish, individual taste cells preferentially express receptors to either L-arginine or L-alanine. In addition, PHA-E binds to the apices of solitary chemoreceptor cells in the epithelium, indicating that this independent chemoreceptor system may utilize some receptor sites similar to those in taste buds.

Alanine↗
PubMed1999

p53 and Bax: putative death factors in taste cell turnover.

The turnover of cells in renewing epithelia presents an opportunity to examine cell death pathways in adult vertebrates. In mouse lingual epithelium a typical taste receptor cell survives for 9 days, until it is killed by an unknown cascade of death factors. Apoptosis was implicated by the presence of fragmented DNA in about 8% of taste receptor cells in the vallate papilla. In using immunocytochemistry to seek putative death factors, we observed that squamous epithelial cells of the tongue were negative for Bax, a death factor in the Bcl-2 family of survival/death factors, and were also negative for p53, a tumor-suppressor protein linked to apoptosis and Bax transcription. In contrast, 8-10% of the taste receptor cells were Bax-positive, and 9-11% were p53 positive. These immunopositive taste receptor cells were more likely to display death-related morphologic defects than other receptor cells, and they frequently coexpressed p53 and Bax. In both neonatal and adult mice, the labeling of dividing cells with 5-bromo-2'-deoxyuridine indicated that all Bax-positive taste cells were at least 5 days old. On postnatal day 7, when few taste cells were old, no more than 1% of taste cells were immunopositive for either p53 or Bax. We inferred that old taste receptor cells employ p53 and Bax as part of their apoptotic death pathway. The routine expression of p53 by postmitotic, aged taste cells broadens the conventional view that p53 is restricted to mitotic cells that have stress-damaged DNA. Furthermore, the scattered distribution of aged receptor cells within the taste bud excludes some explanations for stable taste signals during receptor cell turnover.

Aging↗
PubMed1999

Differential expression of carbohydrate blood-group antigens on rat taste-bud cells: relation to the functional marker alpha-gustducin.

An afferent nerve fiber supplying a taste bud receives input from several taste receptor cells, yet is predominantly responsive to one of the classic taste qualities (salt, acid, sweet, or bitter). This specificity requires recognition between taste receptor cells and nerve fibers that may be mediated by surface markers correlating with function. In an effort to identify potential markers, we used immunofluorescence and confocal microscopy to examine expression of the oligosaccharide blood-group antigens Lewis(b), A, and H type 2 in taste buds of the rat oral cavity. We compared the distributions of these antigens with that of alpha-gustducin, a G-protein subunit implicated in responses to sweet- and bitter-tasting substances. The A and Lewis(b) antigens were present only on spindle-shaped cells whose apical processes reached the taste pore. These antigens were not present on epithelial cells surrounding taste buds, and Lewis(b) was not found elsewhere in the digestive tract. Lewis(b) and A were not removed by lipid extraction, suggesting that they are present on glycoproteins rather than glycolipids. All Lewis(b)-positive cells expressed alpha-gustducin, but only a fraction of alpha-gustducin-positive cells expressed Lewis(b). The fraction of taste-bud cells expressing Lewis(b) decreased in the order: vallate papillae > foliate papillae > nasoincisor duct. The epiglottis had almost no taste-bud cells that expressed Lewis(b). The A antigen appeared on taste-bud cells that also expressed alpha-gustducin in the order: foliate and vallate papillae > nasoincisor duct and epiglottis > fungiform papillae. In addition, the A antigen was present on many cells that lacked alpha-gustducin in foliate and vallate papillae. In vallate papillae, cells expressed either A or Lewis(b), but not both. Lewis(b) appears to be restricted to differentiated light cells that also express alpha-gustducin and may be involved in intercellular interactions of these cells.

Animals↗
PubMed2006

Mice lacking the p75 receptor fail to acquire a normal complement of taste buds and geniculate ganglion neurons by adulthood.

Brain-derived neurotrophic factor and neurotrophin-4 are required for normal taste bud development. Although these neurotrophins normally function via the tyrosine kinase receptor, trkB, they also bind to the pan-neurotrophin receptor, p75. The goal of the present study was to determine whether the p75 receptor is required for the development or maintenance of a full complement of adult taste buds. Mice with p75 null mutations lose 34% of their circumvallate taste buds, 36% of their fungiform papillae, and 26% of their fungiform taste buds by adulthood. The reduction of taste buds in the adult circumvallate papilla was similar to that observed previously at postnatal day 7 (Fan et al. Brain Res Dev Brain Res 2004;150:23-39). Taken together, these findings indicate that the p75 receptor is critical for the development of a full complement of taste buds, but is not required for maintenance of circumvallate taste buds in adulthood. Immunolabeling for p75 was not observed in taste buds, indicating that p75 signaling influences taste bud number indirectly. Geniculate ganglion neurons, which provides innervation to fungiform taste buds, express the p75 receptor. Mice with p75 null mutations also have fewer neurons in the geniculate ganglion. Together, these results suggest that the p75 receptor is important for the survival of geniculate neurons and geniculate neuron survival is required for the development of a full complement of taste buds by adulthood.

Aging↗
PubMed2004

Taste bud cell dynamics during normal and sodium-restricted development.

Taste bud volume increases over the postnatal period to match the number of neurons providing innervation. To clarify age-related changes in fungiform taste bud volume, the current study investigated developmental changes in taste bud cell number, proliferation rate, and life span. Taste bud growth can largely be accounted for by addition of cytokeratin-19-positive taste bud cells. Examination of taste bud cell kinetics with 3H-thymidine autoradiography revealed that cell life span and turnover periods were not altered during normal development but that cells were produced more rapidly in young rats, a prominent modification that could lead to increased taste bud size. By comparison, dietary sodium restriction instituted during pre- and postnatal development results in small taste buds at adulthood as a result of fewer cytokeratin-19-positive cells. The dietary manipulation also had profound influences on taste bud growth kinetics, including an increased latency for cells to enter the taste bud and longer life span and turnover periods. These studies provide fundamental, new information about taste bud development under normal conditions and after environmental manipulations that impact nerve/target matching.

Animals↗
PubMed1993

Transcellular labeling by DiI demonstrates the glossopharyngeal innervation of taste buds in the lingual epithelium of the axolotl.

Innervation of the axolotl lingual epithelium by the glossopharyngeal nerve was examined to reveal its sensory target cells. The carbocyanine dye diI was applied to the nerve stump in the tongue fixed with paraformaldehyde. After a diffusion period of several months, the tongues were examined with a conventional epifluorescence microscope and a confocal laser scanning microscope (LSM) in wholemounts or preparations sectioned with a vibratome. Beneath the epithelium the labeled nerve fibers spread horizontally to form a meshwork of fibers, from which fascicles of fibers extended upward perpendicularly to the epithelium to innervate taste buds. Numerous taste buds were labeled by possible transcellular diffusion of diI. At the base of the taste bud, the nerve fibers branched and formed a basal plexus of fine fibers, on which numerous varicosities were seen. One or at most several taste cells were labeled in a taste bud. In the basal part of taste buds, the cell without an apical process, the basal cell, was also labeled. In the epithelium, between the taste buds, a few solitary cells were labeled. In some cases, a single fascicle of fibers innervating these cells was clearly shown by the LSM. In addition, fine fibers apparently formed free nerve endings in the epithelial cell layer. The results showed that the IX nerve innervated not only taste cells, but also presumed mechanosensory basal cells in the taste bud and the solitary cells of unknown function in the non-taste lingual epithelium. Afferent nerve responses to mechanical stimulation of the tongue may be explained by these non-taste cellular elements in the epithelium.

Ambystoma mexicanum↗
PubMed1994

Expression of the neural cell adhesion molecule (NCAM) and polysialic acid during taste bud degeneration and regeneration.

Taste receptor cells are replaced throughout life, accompanied by continuing synaptogenesis between newly formed taste cells and first-order gustatory fibers. The neural cell adhesion molecule (NCAM) is expressed by a subset of taste cells in adult rodents and appears on gustatory nerve fibers during development prior to differentiation of the taste buds. We employed antibodies against the extracellular domain of the NCAM polypeptide (mAb 3F4) and against polysialic acid (PSA) residues found on embryonic forms of NCAM (mAb 5A5) to investigate the relationship between the expression of these molecules and the innervation of taste buds in adult rats. In unoperated rats, anti-NCAM recognized a subset of cells within the vallate taste buds and also the fibers of the glossopharyngeal (IXth) nerve, including those innervating the gustatory epithelium. Taste bud cells did not express PSA but mAb 5A5 immunoreactivity was observed on some fibers of the IXth nerve, including a few that entered the taste buds. Bilateral crush of the IXth nerve resulted in the loss of NCAM expression from the gustatory epithelium within 8 days. As IXth nerve fibers reinnervated the epithelium, NCAM expression was seen first in the nerve, followed by increased expression in the epithelium as the taste cells differentiated from their precursors. PSA expression by fibers of the IXth nerve did not return to normal until well after the regeneration of the vallate taste buds. The present results demonstrate that taste cell expression of NCAM is dependent upon innervation by the IXth nerve and that NCAM expression appears in the nerve prior to its expression in the differentiating epithelium during regeneration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Taste bud development in the zebrafish, Danio rerio.

Taste buds are chemosensory endorgans consisting of modified epithelial cells. Fish and other vertebrates use their taste bud cells to sample potential food, either selecting or rejecting substances according to their edibility. The adult gustatory system in fish has been studied thoroughly, including regeneration experiments. Taste buds occur in the epithelia of the lips, the mouth cavity, the oropharyngeal cavity, and also in the skin of the barbels, the head, and sometimes even all over the body surface. Despite its importance for feeding, little is known about the ontogeny of the fish taste system. We examined the development of taste buds in the zebrafish on the light microscopical and the scanning and transmission electron microscopical levels. Taste buds develop later than the olfactory organ and the solitary chemosensory cells, two other chemosensory systems in aquatic vertebrates. The first few taste bud primordia are visible within the epithelia of lips and gill arches 3 to 4 days after fertilization, and the first few taste buds with open receptor areas appear on the lips and simultaneously on the gill arches 4-5 days after fertilization, which coincides with the onset of feeding. Taste buds in the mouth cavity, on the head, and on the barbels are formed later in development. As seen in other fish, zebrafish taste buds contain elongate dark and light cells, termed according to their electron density. Dark cells with a cell apex of many short microvilli appear first, followed by the light cells with one large microvillus. In addition, the zebrafish has a third fusiform cell type, which appears last. This cell type is low in electron density and has a brush-like apical ending with several small microvilli. This cell type has not been described previously. Furthermore, in zebrafish, the ontogenetic processes of taste bud formation differ from regenerative processes described in the literature.

Animals↗