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PubMed2002

Localization and functional investigation of the transcription factor CREB in taste receptor cells.

Taste receptor cells utilize the cAMP and other second messenger systems in transducing sweet and bitter stimuli into physiological responses. However, long-term consequences of taste stimulation, such as gene expression, are unknown. We investigated the presence of cAMP response element-binding protein (CREB), a stimulus-induced transcription factor, in taste receptor cells. Using immunocytochemistry, both CREB and its activated form, phosphorylated-CREB (pCREB), were localized to a subset of rat taste receptor cells. Basal level of pCREB was high in the absence of any known stimulation. Using western blot analysis and specific protein kinase inhibitors, CREB phosphorylation was demonstrated to be linked to protein kinase A but not to protein kinase C activation. Stimulation of taste receptor cells with sucrose, a sweet stimulus that elevates cAMP levels, was without effect on CREB phosphorylation. There was a tendency for quinine stimulation, a bitter stimulus that lowers cAMP, to reduce CREB phosphorylation. These results suggested that taste receptor cells express CREB and that its phosphorylation is influenced by the cAMP second messenger system.

Animals↗
PubMed2004

RGS21 is a novel regulator of G protein signalling selectively expressed in subpopulations of taste bud cells.

Abstract G-protein-mediated signalling processes are involved in sweet and bitter taste transduction. In particular, the G protein alpha-subunit gustducin has been implicated in these processes. One of the limiting factors for the time-course of cellular responses induced by tastants is therefore the intrinsic GTPase activity of alpha-gustducin, which determines the lifetime of the active G protein complex. In several signalling systems specific 'regulator of G protein signalling' (RGS) proteins accelerate the GTPase activity of G protein alpha-subunits. Using differential screening approaches, we have identified a novel RGS protein termed RGS21, which represents the smallest known member of this protein family. Reverse transcription polymerase chain reaction and in situ hybridization experiments demonstrated that RGS21 is expressed selectively in taste tissue where it is found in a subpopulation of sensory cells. Furthermore, it is coexpressed in individual taste cells with bitter and sweet transduction components including alpha-gustducin, phospholipase Cbeta2, T1R2/T1R3 sweet taste receptors and T2R bitter taste receptors. In vitro binding assays demonstrate that RGS21 binds alpha-gustducin in a conformation-dependent manner and has the potential to interact with the same Galpha subtypes as T1R receptors. These results suggest that RGS21 could play a regulatory role in bitter as well as sweet taste transduction processes.

Aluminum Compounds↗
PubMed1990

Factors related to the electric taste threshold in type 1 diabetic patients.

To specify the factors related to taste function in Type 1 diabetes mellitus, 50 diabetic out-patients and 50 control subjects paired for age and sex were screened for taste disorders. None of them consumed significant amounts of alcohol, smoked, or had disease or took drugs capable of altering taste. Taste was studied with electrogustometry, retinopathy was detected by fluorescein angiography, nephropathy by measurement of albuminuria and microalbuminuria, peripheral neuropathy by electroneurography and electromyography, and autonomic neuropathy by cardiovascular function tests. The electrogustometric threshold was, on average, significantly higher in the diabetic group (133 +/- 30 microA) than in the control group (29 +/- 9 microA; p less than 0.001). Electric hypogeusia (electrogustometric threshold greater than 100 microA) was found among 54% of the diabetic patients vs 2% of the control subjects (p less than 0.001). In the diabetic group, the electrogustometric threshold was associated with complications of diabetes, especially with peripheral neuropathy (210 +/- 24 vs 90 +/- 22 microA; p less than 0.001) and microalbuminuria (185 +/- 25 vs 86 +/- 21 microA; p less than 0.01). It was correlated with age (r = 0.37; p less than 0.01) and duration of diabetes (r = 0.52; p less than 0.001) but not with HbA1c (r = -0.04). Using multivariate analysis, duration of diabetes and peripheral neuropathy had the strongest association with taste impairment. These results support previous findings, suggesting that taste impairment is a degenerative complication of diabetes mellitus.

Adult↗
PubMed1998

Neural circuits for taste. Excitation, inhibition, and synaptic plasticity in the rostral gustatory zone of the nucleus of the solitary tract.

The rostral nucleus of the solitary tract (rNST) plays a key role in modulating, organizing and distributing the sensory information arriving at the central nervous system from gustatory receptors. However, except for some anatomical studies of rNST synapses, the neural circuits responsible for this first stage in synaptic processing of taste information are largely unknown. Over the past few years we have used an in vitro brain slice preparation of the rNST to study synaptic processing, and it has become apparent that the rNST is a very complex neural relay. Synaptic potentials recorded in rNST neurons resulting from stimulation of afferent taste fibers are a composite of excitatory and inhibitory post synaptic potentials. Pure excitatory postsynaptic potentials (EPSP) can be isolated by using gamma-aminobutyric acid type A (GABAA) receptor blockers to eliminate the inhibitory postsynaptic potentials (IPSP). Application of glutamate ionotropic receptor blockers effectively eliminates all postsynaptic activity, indicating that glutamate is the transmitter at the first central synapse in the taste pathway. Stimulation of the afferent taste fibers originating from the anterior (chorda tympani) and posterior (glossopharyngeal) tongue results in a postsynaptic potential that is a complex sum of the two individual potentials. Thus, rNST neurons receive convergent synaptic input from the anterior and posterior tongue. The IPSP component of the synaptic potentials in rNST results from stimulation of interneurons. If these IPSPs are initiated by tetanic stimulation they undergo both short-term and long-term changes. Short-term changes result in the development of biphasic depolarizing IPSPs, and long-term changes result in potentiation of the IPSPs that can last over an hr in some neurons. This remarkable synaptic plasticity may be involved in the mechanism of learned taste behaviors. Synaptic transmission in rNST consists of excitation combined with inhibition. The inhibition does not simply depress excitation but probably serves many roles such as shaping and limiting excitation, coordinating the timing of synaptic events and participating in synaptic plasticity. Knowledge of these synaptic mechanisms is essential to understanding how the rNST processes taste information.

Animals↗
PubMed2002

Adrenergic signalling between rat taste receptor cells.

In taste buds, synaptic transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the beta agonist isoproterenol and blocked by the beta antagonist propranolol. The alpha agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple alpha (alpha1a, alpha1b, alpha1c, alpha1d, alpha2a, alpha2b, alpha2c) and beta (beta1, beta2) subtypes of adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that adrenergic transmission within the taste bud may play a paracrine role in taste physiology.

Adrenergic alpha-Agonists↗
PubMed1988

A bitter substance induces a rise in intracellular calcium in a subpopulation of rat taste cells.

The sense of taste permits animals to discriminate between foods that are safe and those that are toxic. Because most poisonous plant alkaloids are intensely bitter, bitter taste warns animals of potentially hazardous foods. To investigate the mechanism of bitter taste transduction, a preparation of dissociated rat taste cells was developed that can be studied with techniques designed for single-cell measurements. Denatonium, a very bitter substance, caused a rise in the intracellular calcium concentration due to release from internal stores in a small subpopulation of taste cells. Thus, the transduction of bitter taste may occur via a receptor-second messenger mechanism leading to neurotransmitter release and may not involve depolarization-mediated calcium entry.

Animals↗
PubMed1983

Methyl 4,6-dichloro-4,6-dideoxy-alpha-D-galactopyranoside: an inhibitor of sweet taste responses in gerbils.

The sugar methyl 4,6-dichloro-4,6-dideoxy-alpha-D-galactopyranoside (DiCl-gal) is a new type of inhibitor of the gerbil's electrophysiological taste response to sucrose or saccharin. Saturated solutions of this compound alone barely stimulate the gerbil's taste nerve. But, when mixed with sucrose or saccharin, DiCl-gal suppresses the gerbil's taste response to these two sweeteners. In contrast, when mixed with sodium chloride or hydrochloric acid, DiCl-gal does not affect the taste responses to these compounds. However, unlike other inhibitors of sweet taste, the DiCl-gal taste suppression is short-lived and occurs only when the inhibitor is combined with the sweetener.

Action Potentials↗
PubMed1980

Malrecognition of taste in uremia.

Impaired cognitive functions were reported in uremia. The purpose of this study was to quantify the functional state of taste in various stages of chronic renal failure. Taste sensitivity was assessed by asking the subjects to identify test solutions of sucrose ('sweet'), NaCl ('salty'), citric acid ('sour'), quinine ('bitter') and water presented randomly in five concentrations. The number of recognition errors was statistically analyzed as a measure of taste acuity. Four groups of subjects were examined: 20 nondialyzed uremic patients, 23 patients on regular hemodialysis, 20 patients suffering from chronic diseases with normal renal functions and 22 healthy volunteers. Non dialyzed and dialyzed uremic patients younger than 55 years had a significant impairment of recognition in all taste modalities when compared to both control groups. This was less obvious in patients older than 55 years. No differences in taste recognition were found between dialyzed and nondialyzed uremics of all ages. In the younger age group, however, there was imrpovement in the recognition of 'sour' and 'bitter' when tested before and immediately after the dialysis session. As zinc deficiency was excluded in all of the uremic patients we conclude that the impaired taste perception is another subtle facet of the uremic neuropathy.

Adult↗
PubMed2004

Bitter taste receptors for saccharin and acesulfame K.

Weight-conscious subjects and diabetics use the sulfonyl amide sweeteners saccharin and acesulfame K to reduce their calorie and sugar intake. However, the intrinsic bitter aftertaste, which is caused by unknown mechanisms, limits the use of these sweeteners. Here, we show by functional expression experiments in human embryonic kidney cells that saccharin and acesulfame K activate two members of the human TAS2R family (hTAS2R43 and hTAS2R44) at concentrations known to stimulate bitter taste. These receptors are expressed in tongue taste papillae. Moreover, the sweet inhibitor lactisole did not block the responses of cells transfected with TAS2R43 and TAS2R44, whereas it did block the response of cells expressing the sweet taste receptor heteromer hTAS1R2-hTAS1R3. The two receptors were also activated by nanomolar concentrations of aristolochic acid, a purely bitter-tasting compound. Thus, hTAS2R43 and hTAS2R44 function as cognate bitter taste receptors and do not contribute to the sweet taste of saccharin and acesulfame K. Consistent with the in vitro data, cross-adaptation studies in human subjects also support the existence of common receptors for both sulfonyl amide sweeteners.

Aristolochic Acids↗
PubMed2005

Expression of synaptotagmin 1 in the taste buds of rat gustatory papillae.

Synapses between taste receptor cells and primary sensory afferent fibers transmit the output signal from taste buds to the central nervous system. The synaptic vesicle cycle at the synapses involves vesicle docking, priming, fusion, endocytosis, and recycling. Many kinds of synaptic vesicle proteins participate in synaptic vesicle cycles. One of these, synaptotagmin 1, binds Ca(2+) phospholipids with high affinity and plays a role in Ca(2+) regulated neurotransmitter release in the central and peripheral nervous systems. However, the expression patterns of synaptotagmin 1 in rat taste tissues have not been determined. We therefore examined the expression patterns of synaptotagmin 1 and several cell specific markers of type II and III cells in rat taste buds. RT-PCR assay showed that synaptotagmin 1 mRNA was expressed in circumvallate papillae. In fungiform, foliate, and circumvallate papillae, the antibody against synaptotagmin 1 yielded the labeling of a subset of taste bud cells and intra- and subgemmal nerve processes. Double labeled experiments showed that synaptotagmin 1 positive cells co-expressed type III cell markers, PGP 9.5, and NCAM. Intragemmal nerve processes positive for synaptotagmin 1 co-expressed PGP 9.5. Conversely, all synaptotagmin 1 expressing cells did not co-expressed type II cell markers, PLCbeta2, or gustducin. These results show that synaptotagmin 1 may play some regulatory roles in vesicle membrane fusion events with the plasma membrane at the synapses of type III cells in rat taste buds.

Animals↗
PubMed1993

Taste and odor: reactivity in depressive disorders, a multidisciplinary approach.

Depressive patients often complain about dullness of taste of previously liked food items as well as of persistent bad taste. Taste and smell experience can be reflected by cognitive (psychophysical) indicators and also by reflectory (facial expressive) responses. In the present study 21 depressed, hospitalized patients and 16 control subjects were exposed to food-related gustatory and olfactory stimuli. Psychophysical and videotaped facial reactions were recorded from both groups. Analysis indicated that cognitive estimates of taste hedonics were similar for depressed and control groups; the former responded to sweet taste with a shorter-lasting facial reaction, involving markedly fewer facial features expressing enjoyment, than did controls. Aversive tastes, in contrast, triggered comparable facial expressive features of disgust in both groups. Facial reactions of depressed patients to acceptable and aversive olfactory stimuli were all significantly shorter and more muted than those of controls. Facial reflexes triggered by chemical cues are known to be controlled primarily by brainstem structures. Present findings suggest a possible influence of the profound anhedonia of severe depression on subcortical processes.

Adult↗
PubMed1999

A confusion matrix for the study of taste perception.

Taste stimulus identification was studied in order to more thoroughly examine human taste perception. Ten replicates of an array of 10 taste stimuli--NaCl, KCl, Na glutamate, quinine. HCl, citric acid, sucrose, aspartame, and NaCl-sucrose, acid-sucrose, and quinine-sucrose mixtures--were presented to normal subjects for identification from a list of corresponding stimulus names. Because perceptually similar substances are confused in identification tasks, the result was a taste confusion matrix. Consistency of identification for the 10 stimuli (T10) and for each stimulus pair (T2) was quantified with measures derived from information theory. Forty-two untrained subjects made an average of 57.4% correct identifications. An average T10 of 2.25 of the maximum 3.32 bits and an average T2 of 0.84 of a maximum 1.0 bit of information were transmitted. In a second experiment, 40 trained subjects performed better than 20 untrained subjects. The results suggested that the identification procedure may best be used to assess taste function following 1-2 training replicates. The patterns of taste confusion indicate that the 10 stimuli resemble one another to varying extents, yet each can be considered perceptually unique.

Adolescent↗
PubMed1999

Taste buds and neuronal markers in patients with chronic renal failure.

OBJECTIVE: To study the number of taste buds and, with the use of specific markers for peripheral nervous tissue, to study the neuronal pattern in taste buds from 36 patients with chronic renal failure (CRF), 19 renal transplant recipients, and 40 healthy subjects. Of the patients with CRF, 17 patients had not started dialysis, 12 patients were on peritoneal dialysis, and 7 patients were on hemodialysis. DESIGN: From all subjects, two or three fungiform papillae were collected from the anterior part of the tongue. Cryostat sections were cut and inspected under light microscopy to determine the presence of taste buds. The sections were subsequently incubated with primary rabbit antibodies against protein gene product 9.5, substance P, and nerve growth factor receptor. RESULTS: Using these antibodies, no differences between the groups were observed. However, patients with CRF had fewer taste buds than control subjects. CONCLUSION: No immunohistochemical differences were observed between patients with CRF and healthy controls. However, patients with CRF had significantly fewer fungiform taste buds, suggesting an important factor contributing to the well-known impairment of taste acuity in this patient group.

Adult↗
PubMed2000

Smell and taste disorders: a primary care approach.

Smell and taste disorders are common in the general population, with loss of smell occurring more frequently. Although these disorders can have a substantial impact on quality of life and may represent significant underlying disease, they are often overlooked by the medical community. Patients may have difficulty recognizing smell versus taste dysfunction and frequently confuse the concepts of "flavor" and "taste." While the most common causes of smell disturbance are nasal and sinus disease, upper respiratory infection and head trauma, frequent causes of taste disturbance include oral infections, oral appliances (e.g., dentures), dental procedures and Bell's palsy. Medications can interfere with smell and taste, and should be reviewed in all patients with reported dysfunction. In addition, advancing age has been associated with a natural impairment of smell and taste ability. A focused history and a physical examination of the nose and mouth are usually sufficient to screen for underlying pathology. Computed tomographic scanning or magnetic resonance imaging of affected areas, as well as commercially available standardized tests, may be useful in selected patients. The causes of olfactory dysfunction that are most amenable to treatment include obstructing polyps or other masses (treated by excision) and inflammation (treated with steroids). Enhancement of food flavor and appearance can improve quality of life in patients with irreversible dysfunction.

Age Factors↗
PubMed1992

Taste alterations in liver cirrhosis: are they related to zinc deficiency?

Patients with chronic liver disease may have taste impairment and altered zinc metabolism. We evaluated Taste Detection Thresholds (TDTs) in 60 patients with liver cirrhosis and correlated the findings with disease severity and alcoholic etiology. Plasma zinc levels and urinary output were also measured. A placebo-controlled treatment trial with zinc sulphate was made in 15 patients with compensated cirrhosis in order to ascertain whether zinc deficiency caused taste alterations. Taste detection of salty, sweet and acid tastants was significantly impaired in all cirrhotic patients in comparison with normal subjects. TDTs were not influenced either by the etiology or the severity of the disease. All groups of patients had low plasma zinc levels and decompensated cirrhosis had a significantly increased urinary output of zinc. No correlation was found between taste acuity and plasma zinc levels when only cirrhotic patients were considered. The effect of zinc supplementation on TDTs did not appear to be inferior to that of the placebo. Our results indicate that taste impairment in cirrhotics is due to the disease process per se and not to zinc deficiency.

Adult↗
PubMed2006

[The sense of taste].

The taste sense is one of the five human senses. It is essential to our survival because it enables the individual the choice of correct food, which, in turn, is crucial for one's existence, maintenance and function. This is a complicated chemical sense, which operates in conjunction with other senses such as vision, smell and touch, and is also associated with the operation of temperature and consistency receptors. There are five basic tastes: bitter, sweet, sour, salty and "fleshy" (umami), each of which has a role in food selection, being responsible for the recognition of certain chemicals, which may be either necessary or dangerous to our body. The taste cell is located in the taste buds, which, in turn, are situated in the tongue, oral cavity and the proximal third of the esophagus. This translates the chemical signal of tastants in food to electrical stimulation that transfers the signal to higher processing centers in the brain, in a process called transduction, which is explained in this review. Disturbances in the taste sense, as well as effects of industrial exposure on this sense are also described. The accumulated knowledge about the taste sense might enable future breakthroughs in the processed food industry.

Brain↗
PubMed1989

[Clinical study of taste abnormalities in advanced lung cancer cases].

Taste recognition thresholds for four basic tastes, sweet, salty, and bitter, have been examined in 36 advanced lung cancer patients to identify the presence or absence of taste abnormalities in such patients. Twenty-six untreated lung cancer patients, or 65.3%, demonstrated an abnormal taste threshold for at least one of the 4 taste, a result varying significantly from suitable controls (p less than 0.05). Among the total 36 lung cancer patients, the number of those showing a threshold abnormality was no different between the smoker and non-smoker groups, though abnormalities were higher in the low serum zinc level group than in the normal serum zinc level group (p less than 0.05). We also observed transient threshold elevations after chemotherapy including Cisplatin. Thus, it is thought that taste abnormalities are more prevalent in advanced lung cancer patients.

Adult↗
PubMedDate not supplied

[Electrometric method of studying taste in brain diseases].

Disorders of the sense of taste were studied in 355 patients with craniocerebral pathology, among whom 70 had tumors of the acoustic nerve, 64 had a craniocerebral trauma, 60 had tumors of the cerebral hemispheres. The most coarse disorders with the loss of the sense of taste on the anterior 2/3 of the tongue were encountered in tumors of the acoustic nerve and in transverse infracture of the pyramid of the temporal bone. Longitudinal infractures of the pyramid usually cause a diminished sense of taste on the anterior 2/3 of the tongue in the acute period, with improvment of the taste in the late periods after the trauma. The test for the sense of taste on the anterior 2/3 of the tongue in tumors of the acoustic nerve, in infractures of the temporal bone pyramid, and in arachnoiditis of the cerebellopontine angle is one of the diagnostic methods. Electrogustometry makes it possible to detect the earliest disorders in the sense of taste and make a more precise diagnosis.

Arachnoiditis↗