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PubMed2000

Neuron/target matching between chorda tympani neurons and taste buds during postnatal rat development.

During postnatal development, a relationship is established between the size of individual taste buds and number of innervating neurons. To determine whether rearrangement of neurons that innervate taste buds establishes this relationship, we labeled single taste buds at postnatal day 10 (P10) and again at either P15, P20, or P40 with retrograde fluorescent neuronal tracers. The number of single- and double-labeled geniculate ganglion cells was counted, and the respective taste bud volumes were measured for the three groups of rats. The current study replicates findings from an earlier report demonstrating that the larger the taste bud, the more geniculate ganglion cells that innervate it. This relationship between taste bud size and number of innervating neurons is not apparent until P40, when taste bud size reaches maturity. These findings are extended here by demonstrating that the number of neurons that innervate taste buds at P10, when taste bud size is small and relatively homogeneous, predicts the size that the respective taste bud will become at maturity. Moreover, while there is some neural rearrangement of taste bud innervation from P10 to P40, rearrangement does not impact the relationship between taste bud size and innervating neurons. That is, the neurons that maintain contact with taste buds from P10 through P40 accurately predict the mature taste bud size. Therefore, the size of the mature taste bud is determined by P10 and relates to the number of sensory neurons that innervate it at that age and the number of neurons that maintain contact with it throughout the first 40 days of postnatal development.

Age Factors↗
PubMed1987

A sensitive period for the neural induction of taste buds.

Taste buds mature postnatally in the vallate papilla of the rat and reach a mean number of 610 by day 90. Although taste buds are neurotrophically dependent, the presence of widespread bilateral innervation permits more than 80% of the 610 vallate taste buds to survive after one IXth nerve is removed in adults. However, after a IXth nerve is removed at 0-3 d postpartum, about two-thirds of the vallate taste buds fail to develop. In the present investigation, the timing of the neural induction of taste buds was examined by unilaterally removing the IXth nerve at 12 different postnatal ages, from 0 to 75 d. Unilateral denervation revealed the existence of a sensitive period that is maximal from 0 to 10 d, when unilateral or bilateral interruption of the IXth nerve profoundly impairs the formation of taste buds. The number of taste buds that form is nonlinearly dependent upon the number of axons; at low levels of innervation, a doubling of the number of myelinated axons quintuples the number of taste buds. Thus, taste axons interact synergistically. In studying regeneration, we found that axons of both neonatal and adult IXth nerves elongate approximately 1.8 mm/d. Taste buds were re-formed more rapidly and a higher proportion were bilaterally innervated when regenerating axons and the sites of former taste buds were numerous. The proportion of bilaterally innervated taste buds could be approximated from the likelihood of random overlap of axons from the right and left IXth nerves. The greater ease with which taste buds are re-formed than developed suggests that taste bud regeneration does not recapitulate taste bud development.

Animals↗
PubMed2002

Taste dysfunction in irradiated patients with head and neck cancer.

Taste disorders caused by radiation therapy for head and neck cancer are common. This prospective study of 40 patients with head and neck cancer assessed changes in taste sensations during radiation therapy. The relationship between the time course and the degree of taste disorder was studied. The taste recognition threshold and supra-threshold taste intensity performance for the four basic tastes were measured using the whole-mouth taste method before, during, and after radiation therapy. Bitter taste was affected most. An increase in threshold for sweet taste depended upon whether the tip of tongue was included within the radiation field. The slope of the taste intensity performance did not change during or after radiotherapy. The pattern of salivary dysfunction was different from that of taste dysfunction. The main cause of taste disorders during radiation support the hypothesis that taste dysfunction is due to damage to the taste buds in the radiation field.

Adult↗
PubMed1994

Taste Acuity of the Morbidly Obese before and after Gastric Bypass Surgery.

Obese individuals have an increased preference for high caloric foods, such as sweets and fats. However, following gastric bypass (GBP) surgery, morbidly obese patients tend to avoid these foods. We hypothesize that this aversion may occur, in part, from permutations in taste acuity. To test this hypothesis, taste detection and recognition thresholds for the four basic tastes (salt, sweet, sour, and bitter) were assessed using a modification of the Henkin forced choice three stimulus technique. Taste acuity measurements were obtained at baseline and at 30, 60, and 90 days post-operative for six morbidly obese GBP women and ten non-surgical, lean female controls. We found nonsignificant differences in taste detection and recognition thresholds between morbidly obese and lean control study subjects at baseline, and no significant correlation between taste acuity and body size. Furthermore, in our study population of lean and obese women, ages 26 to 52, there were no significant interrelationships between baseline taste thresholds and known effectors of taste acuity, i.e., zinc levels, glycemic status, liver and kidney function, or age. Following GBP surgery, a significant up-regulation in taste acuity for bitter and sour was observed along with a trend toward a reduction in salt and sweet detection and recognition thresholds. These findings would suggest the following: (1) taste acuity does not influence taste preferences of the obese individual who has not had bariatric surgery; (2) taste effectors such as zinc, when within the range of normal values, do not alter thresholds of the 4 basic tastes; and (3) weight loss following gastric bypass surgery is associated with an up-regulation in taste acuity in the morbidly obese. Studies are currently under investigation at our center to identify the specific etiology of taste acuity upregulation in the morbidly obese following GBP surgery.

Journal Article↗
PubMed2003

(+)-(S)-alapyridaine--a general taste enhancer?

N-(1-Carboxyethyl)-6-hydroxymethyl-pyridinium-3-ol inner salt (alapyridaine), recently identified in heated sugar/amino acid mixtures as well as in beef bouillon, has been shown to exhibit general taste-enhancing activities, although tasteless on its own. Differing from other taste enhancers reported so far, racemic (R/S)-alapyridaine and, to an even greater extent (+)-(S)-alapyridaine, the physiologically active enantiomer, are able to enhance more than one basic taste quality. The threshold concentrations for the sweet taste of glucose and sucrose, for the umami taste of monosodium L-glutamate (MSG) and guanosine-5'-monophosphate (GMP), as well as the salty taste of NaCl, were significantly decreased when alapyridaine was present. In contrast, perception of the bitter tastes of caffeine and L-phenylalanine, as well as of sour-tasting citric acid, was unaffected. Furthermore, alapyridaine was shown to intensify known taste synergies such as, for example, the enhancing effect of L-arginine on the salty taste of NaCl, as well as that of GMP on the umami taste of MSG. The activity of (+)-(S)-alapyridaine could be observed not only in solutions of single taste compounds, but also in more complex tastant mixtures; for example, the umami, sweet and salty taste of a solution containing MSG, sucrose, NaCl and caffeine was significantly modulated, thus indicating that alapyridaine is a general taste enhancer.

Adult↗
PubMed2005

Objective assessment of terbinafine-induced taste loss.

OBJECTIVES: Terbinafine (Lamisil), a widely prescribed oral antifungal agent, reportedly induces taste loss in 0.6% to 2.8% of those taking the drug. However, many so-called taste problems reflect olfactory problems, and the sole empirical study published on this topic, based on whole-mouth testing of a single subject, found no terbinafine-related deficit. In this study, we quantitatively assessed, using well-validated taste and smell tests, chemosensory function in six patients complaining of taste disturbance after terbinafine treatment and compared their test scores to those of six age-, race-, and sex-matched normal controls. METHODS: Taste function was measured using a 96-trial regional test that assesses sweet, sour, bitter, and salty taste perception within the anterior (cranial nerve [CN] VII) and posterior (CN IX) lingual taste bud fields. Smell function was bilaterally evaluated using the 40-item University of Pennsylvania Smell Identification Test. RESULTS: Taste function for sweet-, sour-, and bitter-tasting stimuli was significantly depressed in both the anterior and posterior lingual regions. For sodium chloride, the decrements were confined to the posterior region. Olfactory function was within normal limits. CONCLUSION: These findings 1) support anecdotal case reports of taste loss after terbinafine use, 2) demonstrate that all four major taste qualities are affected, and 3) suggest that olfactory dysfunction is not involved. Because self-report markedly underestimates chemosensory deficits, more extensive quantitative testing of patients receiving terbinafine will likely reveal a much higher prevalence of terbinafine-induced taste loss than currently reported. Since being older than 65 years of age and having a low body mass index are reportedly risk factors for terbinafine-induced taste loss, physicians should be particularly on the alert for elderly persons taking this medication who may become depressed or alter their food intake in response to decreased taste sensation.

Adult↗
PubMed1995

[Healing process of taste receptor disturbance].

Patients with taste receptor disturbance were treated with zinc dosage, and their healing process was traced through the filter-paper-disc method and electrogustometry. The number of cases studied was 119,45 with idiopathic taste disturbance, 38 with drug-induced taste disturbance and 36 with zinc-deficient taste disturbance. 1) Three patterns of taste recovery were observed on the tongue surface. Out of a total of 119 cases, 54 cases (45.4%) were found to be improving on the anterior as well as posterior parts of the tongue simultaneously (simultaneous improvement type). Fifty-three cases (44.5%) showed recovery in the posterior part of the tongue (area of the glossopharyngeal nerve) earlier than in other parts of the tongue (posterior improvement type). Only 12 cases (10.1%) showed recovery in the anterior part of the tongue (area of the chorda tympani nerve) earlier than in other parts of the tongue (anterior improvement type), a significantly smaller number of cases compared with the other two types. In particular, very few cases of zinc deficient taste disturbance belonged to the anterior improvement type. Zinc dosage treatment proved to be more rapidly effective for the simultaneous improvement type. 2) With respect to differences in the recovery process of the four primary tastes, a tendency for the sweet and bitter taste qualities to recover earlier than the others was observed in the simultaneous improvement type. However, no phenomenon was observed that could support the existence of the so-called "tongue map", such as the bitter and sour taste recover first among the posterior improvement type or the sweet taste improving first among the anterior improvement type. 3) The results of this study revealed that the treatment of taste receptor disturbances starts with the posterior part of the tongue, which abounds in taste buds. 4) The study also demonstrated that electrogustometry is not suitable for tracing the process of taste receptor disturbance. 5) When tracing the effectiveness of treatment of taste receptor disturbance through the filter paper-disc method, it is sufficient to measure only the posterior part of the tongue (area of the glossopharyngeal nerve) until signs of healing appear.

Adolescent↗
PubMed1996

Temporal and spatial patterns of tenascin and laminin immunoreactivity suggest roles for extracellular matrix in development of gustatory papillae and taste buds.

Gustatory papillae are complex organs that are composed of 1) an epithelium, 2) specialized sensory cells within the epithelium (the taste buds), 3) a broad connective core, and 4) sensory innervation. During papilla development, cells in the various tissue compartments must divide, aggregate, detach, migrate, and reaggregate in relation to each other, but factors that regulate such steps are poorly understood and have not been extensively studied. All of these processes potentially require participation of the extracellular matrix. Therefore, we have studied temporal and spatial patterns of immunoreactivity for two extracellular matrix molecules, tenascin and laminin, in the developing fungiform and circumvallate papillae of fetal, perinatal, and adult sheep tongue. To determine relations of tenascin and laminin to sensory innervation, we used an antibody to growth-associated protein (GAP-43) to label growing nerves. Immunocytochemical distributions of tenascin and laminin alter during development in a manner that reflects morphogenesis rather than histologic boundaries of the taste papillae. In early fungiform papillae, tenascin immunoreactivity is very weak within the mesenchyme of the papilla core. However, there is a subsequent shift to an intense, restricted localization in the apical papilla core only--directly under taste bud-bearing regions of the papilla epithelium. In early circumvallate papillae, tenascin immunoreactivity is patchy within the papilla core and within the flanking, nongustatory papillae. Later, immunoreactivity is restricted to the perimeter of the central papilla core, under epithelium that contains developing taste buds. In fungiform and circumvallate papillae, the shift in tenascin immunolocalization is associated with periods of taste bud formation and multiplication within the papilla epithelium and with extensive branching of the sensory innervation in the papilla apex. Laminin immunoreactivity, although it is continuous throughout the basement membrane of general lingual epithelium, is interrupted in the epithelial basement membrane of early fungiform and circumvallate papillae in regions where taste buds are forming. The breaks are large in young fetuses, when taste buds first develop, and are evidenced later as punctate disruptions. Heparan sulfate proteoglycan immunoreactivity confirms that these are basement membrane discontinuities. GAP-43 label coincides with innervation of the papilla core and is most extensive in regions where tenascin immunoreactivity is weak or absent. GAP-43 immunoreactivity is also found in early taste buds: Later, it is extensive within more mature multiple taste buds, presumably in relation to synaptogenesis. We propose that tenascin has a role in promoting deadhesion of cells in the papilla epithelium during periods of taste bud formation and multiplication. Discontinuities in the epithelial basement membrane under developing taste buds, indicated with laminin and heparan sulfate proteoglycan immunoreactivity, may interact to facilitate taste bud morphogenesis and multiplication, to permit access of papilla innervation to the forming taste buds, and/or to allow epithelial/mesenchymal interactions during papilla and taste bud development.

Animals↗
PubMed2001

Ultrastructure of the taste buds in the blind cave fish Astyanax jordani ("Anoptichthys") and the sighted river fish Astyanax mexicanus (Teleostei, Characidae).

This study describes the ultrastructure of the taste buds of the sighted river fish Astyanax mexicanus and of the blind cave fish Astyanax jordani (= Anoptichthys) (Teleostei, Characiformes, Characidae). In Astyanax and Anoptichthys, taste buds occur in the epithelia of the lips, oral cavity, and, in Anoptichthys, lower jaw. Both possess three types of taste buds: type I (elevated), type II (slightly elevated), and type III taste buds (not elevated or sunken). The taste buds are up to 60 microm high and up to 35 microm wide. The taste bud's sensory epithelium consists of 100--130 elongated cells: light cells, dense-cored-vesicles (dcv) -cells, dark cells, and degenerating cells. The dcv-cells are rich in dense-cored vesicles and are described for the first time in a teleostean taste bud. At the taste bud's base, there lie two to three basal cells. The basal cells of type I and type II taste buds have microvillus (spine)-like processes, in contrast to those of type III taste buds. The taste bud's nerve fiber plexus is situated between the bases of the elongated taste bud cells and the basal cells. Afferent synapses occur between dcv-cells and basal cells (presynaptic sides) and axons (postsynaptic side). Indistinct synapses occur between light cells and dark cells (presynaptic sides) and axons (postsynaptic side). The nerve fiber plexes of Anoptichthys type II and type III taste buds contain significantly more axon profiles than those of Astyanax. This may be associated with a compensatory improvement of the sense of taste in the blind, cave-dwelling fish.

Animals↗
PubMed2004

Synaptobrevin-2-like immunoreactivity is associated with vesicles at synapses in rat circumvallate taste buds.

Synaptobrevin is a vesicle-associated membrane protein (VAMP) that is believed to play a critical role with presynaptic membrane proteins (SNAP-25 and syntaxin) during regulated synaptic vesicle docking and exocytosis of neurotransmitter at the central nervous system. Synaptic contacts between taste cells and nerve processes have been found to exist, but little is known about synaptic vesicle docking and neurotransmitter release at taste cell synapses. Previously we demonstrated that immunoreactivity to SNAP-25 is present in taste cells with synapses. Our present results show that synaptobrevin-2-like immunoreactivity (-LIR) is present in approximately 35% of the taste cells in rat circumvallate taste buds. Synaptobrevin-2-LIR colocalizes with SNAP-25-, serotonin-, and protein gene product 9.5-LIR. Synaptobrevin-2-LIR also colocalizes with immunoreactivity for type III inositol 1,4,5-triphosphate receptor (IP3R3), a taste-signaling molecule in taste cells. All IP3R3-LIR taste cells express synaptobrevin-2-LIR. However, approximately 27% of the synaptobrevin-2-LIR taste cells do not display IP3R3-LIR. We believe, based on ultrastructural and biochemical features, that both type II and type III taste cells display synaptobrevin-2-LIR. All of the synapses that we observed from taste cells onto nerve processes express synaptobrevin-2-LIR, as well as some taste cells without synapses. By using colloidal gold immunoelectron microscopy, we found that synaptobrevin-2-LIR is associated with synaptic vesicles at rat taste cell synapses. The results of this study suggest that soluble NSF attachment receptor (SNARE) machinery may control synaptic vesicle fusion and exocytosis at taste cell synapses.

Animals↗
PubMed2005

Distinct expression pattern of insulin-like growth factor family in rodent taste buds.

The insulin-like growth factor (IGF) system is an important regulator of growth and differentiation in a variety of tissues. In the present study, the expression of IGF family members in the taste buds of mice and rats was examined. By reverse transcriptase polymerase chain reaction (RT-PCR) analysis, mRNA of IGF-I and -II, IGF-I receptor (IGF-IR), insulin receptor (insulin R), and IGF-binding protein (IGFBP)-2, -3, -4, -5, and -6 was detected in the taste bud-containing epithelium of the circumvallate papillae of mice. As suggested by the study using degenerate PCR (McLaughlin [2000] J. Neurosci. 20:5679-5688), IGF-IR was expressed in most of the taste bud cells of adult mice, as found by immunohistochemistry, and in those of postnatal day (P) 6 mice by in situ hybridization. Insulin R, which has strong homology to IGF-IR, was also detected in most of the taste bud cells of mice by immunohistochemistry and in situ hybridization. IGF-I immunoreactivity was detected in a few taste bud cells and in the epithelium surrounding taste buds. Northern blot analysis revealed that the amount of IGF-I mRNA in taste bud-containing epithelium was very low compared with that in liver. IGF-II immunoreactivity was weakly detected in mouse taste buds and the surrounding epithelium. In the rat tissue, a subset of the taste bud cells was positive for IGF-II. Among the six IGFBPs, IGFBP-2, -5, and -6 were detected in the mouse taste buds: IGFBP-2 and -5 immunoreactivity was seen in the majority of the taste bud cells, whereas IGFBP-6 immunoreactivity was found in the nerve fibers innervating the taste buds. In situ hybridization study also revealed that IGFBP-2 and -5 mRNA was synthesized in the taste buds of P6 mice and that the expression of these mRNAs overlapped in von Ebner's glands. These data reveal that IGF-I and -II might be produced in taste bud cells and (or) surrounding lingual epithelium and act through IGF-IR and insulin R locally in a paracrine and autocrine manner. The activity of these IGFs may be modulated through their interaction with IGFBP-2, -5, and 6.

Age Factors↗
PubMed2005

Effects of glossopharyngeal nerve section on the expression of neurotrophins and their receptors in lingual taste buds of adult mice.

The expression of neurotrophins and neurotrophin receptors is essential for the proper establishment and function of many sensory systems. To determine which neurotrophins and neurotrophin receptors are expressed in taste buds, and in taste buds of mice following denervation, antibodies directed against the neurotrophins and their receptors were applied to adult mouse gustatory tissue. Immunohistochemistry reveals that nerve growth factor (NGF)-like immunoreactive (LIR), tyrosine kinase (trk) A-LIR, trkB-LIR, and p75-LIR elongated, differentiated taste cells are present within all lingual taste buds, whereas neither neurotrophin (NT)-3- nor trkC-LIR was detected in taste cells. Double-label immunohistochemistry using markers of different taste cell types in brain-derived neurotrophic factor (BDNF)LacZ mice reveals that BDNF (beta-gal) and trkB colocalize, mainly in type III taste cells. NGF, pro-NGF, and trkA coexist in type II taste cells, i.e., those expressing phospholipase Cbeta2 (PLCbeta2). p75-LIR also is present in both BDNF and NGF taste cell populations. To determine the neural dependence of neurotrophin expression in adult taste buds, glossopharyngeal nerves were cut unilaterally. During the period of denervation (10 days to 3 weeks), taste buds largely disappear, and few neurotrophin-expressing cells are present. Three weeks after nerve transection, nerve fascicles on the operated side of the tongue exhibit BDNF-LIR, NGF-LIR, and ubiquitin carboxyl terminal hydrolase (PGP 9.5)-LIR. However, BDNF-LIR staining intensity but not NGF-LIR or PGP 9.5-LIR is increased in nerve fascicles on the operated compared with the unoperated side. Five weeks following nerve transection, NT and NT receptor expression resumes and appears normal in taste buds and nerves. These results indicate that neurotrophin expression in taste buds is dependent on gustatory innervation, but expression in nerves is not dependent on contact with taste buds.

Animals↗
PubMed1987

Response properties of the parabrachio-thalamic taste and mechanoreceptive neurons in rats.

A total of 66 taste and 33 mechanoreceptive neurons were isolated from the parabrachial nucleus (PB) of rats. Among them, 39 taste and 8 mechanoreceptive neurons were identified as parabrachio-thalamic relay (P-T) neurons on the basis of antidromic activation from either or both sides of the thalamic taste areas (TTAs). On average, the P-T taste neurons produced larger response magnitudes than the non-P-T taste neurons, and whereas about half the P-T taste neurons were NaCl-best, only a small number of the non-P-T taste neurons were NaCl-best. Both the P-T and non-P-T taste neurons showed a similar breadth of responsiveness to four basic taste stimuli. The response magnitudes of the P-T taste neurons to all taste stimuli were ca. 3 times larger than those of the solitario-parabrachial relay (SP) neurons (afferents to the PB); in particular, the response magnitudes of the NaCl-best P-T neurons were 4-5 times larger than those of the NaCl-best SP neurons. The response magnitudes and breadth of taste responsiveness of the P-T taste neurons were reciprocally correlated with the antidromic latencies from either side of the TTAs. A histological examination revealed that the P-T taste neurons in the ventral part of the PB had a shorter antidromic latency from the ipsilateral TTA than those in the dorsal part of the nucleus. Mechanoreceptive neurons were excited by stroking the tissue in the oral cavity or perioral tissue, or by pinching them with non-serrated forceps. The mechanoreceptive P-T neurons were also activated from either or both sides of the TTAs. No particular relation was noticed between the antidromic latency of the mechanoreceptive P-T neurons and their response properties or locations in the nucleus.

Afferent Pathways↗
PubMed2004

Irradiation impairment of umami taste in patients with head and neck cancer.

BACKGROUND: Previous studies have reported the alteration of the four basic tastes (sweet, salty, sour and bitter) in patients with head and neck cancer (HNC) during radiotherapy. However, there has been no investigation on the function of umami taste, a novel basic taste recognized recently, during head and neck irradiation. OBJECTIVE: To investigate the recognition threshold of umami and the four basic tastes at different irradiation dose intervals during radiotherapy for head and neck cancer. METHODS: In 30 patients with malignant neoplasm of head and neck, objective taste thresholds were examined by use of a whole-mouth method at pre-radiotherapy, irradiation doses at 15, 30, 45, and 60 Gy, respectively. Subjective taste loss and some distresses were recorded simultaneously. RESULTS: Sweet, sour, salty, and bitter tastes showed temporarily and slightly increased thresholds during the treatment, but no statistical difference was found between the threshold at pre-radiotherapy and that at 15, 30, 45, and 60 Gy in any taste quality (all P > 0.05). Significantly impaired threshold of umami taste was revealed at 30 Gy (P < 0.05) and remained throughout the following treatment (at 45 and 60 Gy, both P < 0.01). Subjective taste impairment, appetite loss and satisfaction with the current state tended to deteriorate significantly during the irradiation. Mean body weight of the patients experienced a continuous loss, decreasing from an average of 60.4 kg before treatment to 57.3 kg at 60 Gy (P < 0.01). Scores of satisfaction with current state showed a significant correlation with umami taste thresholds (P = 0.035). CONCLUSION: The clinical impairment pattern of umami taste is different from that of the other four basic tastes in HNC patients during radiotherapy. Impaired umami taste acuity plays an important role in impacting the quality of life of the patients irradiated to the head and neck.

Head and Neck Neoplasms↗
PubMed2006

Taste masking analysis in pharmaceutical formulation development using an electronic tongue.

The purpose of this study is to assess the feasibility for taste masking and comparison of taste intensity during formulation development using a multichannel taste sensor system (e-Tongue). Seven taste sensors used in the e-Tongue were cross-selective for five basic tastes while having different sensitivity or responsibility for different tastes. Each of the individual sensors concurrently contributes to the detection of most substances in a complicated sample through the different electronic output. Taste-masking efficiency was evaluated using quinine as a bitter model compound and a sweetener, acesulfame K, as a bitterness inhibitor. In a 0.2 mM quinine solution, the group distance obtained from e-Tongue analysis was reduced with increasing concentration of acesulfame K. This result suggests that the sensors could detect the inhibition of bitterness by a sweetener and could be used for optimization of the sweetener level in a liquid formulation. In addition, the bitterness inhibition of quinine by using other known taste-masking excipients including sodium acetate, NaCl, Prosweet flavor, and Debittering powder or soft drinks could be detected by the e-Tongue. These results further suggest that the e-Tongue should be useful in a taste-masking evaluation study on selecting appropriate taste-masking excipients for a solution formulation or a reconstitution vehicle for a drug-in-bottle formulation. In another study, the intensity of the taste for several drug substances known to be bitter was compared using the e-Tongue. It was found that the group distance was 695 for prednisolone and 686 for quinine, which is much higher than that of caffeine (102). These results indicate that the taste of prednisolone and quinine is stronger or more bitter than that of caffeine as expected. Based on the group distance, the relative intensity of bitterness for these compounds could be ranked in the following order: ranitidine HCl>prednisolone Na>quinine HCl approximately phenylthiourea>paracetamol>>sucrose octaacetate>caffeine. In conclusion, the multichannel taste sensor or e-Tongue may be a useful tool to evaluate taste-masking efficiency for solution formulations and to compare bitterness intensity of formulations and drug substances during pharmaceutical product development.

Biosensing Techniques↗
PubMedDate not supplied

Artificial neural networks estimate the contribution of taste neurons to coding.

Taste qualities are believed to be coded in the activity of populations of taste neurons. However, it is not clear whether all neurons are equally responsible for coding. To clarify the point the relative contribution of each taste neuron to coding was assessed by constructing simple three-layer neural networks with input neurons that represent cortical taste neurons of the rat. The networks were trained by the back-propagation learning algorithm to classify the neural response patterns to the basic taste stimuli (sucrose, HCl, quinine-hydrochloride, and NaCl). The networks had four output neurons representing the basic taste qualities, the values of which provide a measure for similarity of test stimuli to the basic taste stimuli. We estimated relative contributions of input neurons to the taste discrimination of the network by examining their significance S(j), which is defined as the sum of the absolute values of the connection weights from the jth input neuron to the hidden layer. When the input neurons with a smaller S(j) (e.g., 15 out of 39 input units) were "pruned" from the trained network, the ability of the network to discriminate the basic taste qualities was not greatly affected. On the other hand, the taste discrimination of the network progressively deteriorated much more rapidly with pruning of input neurons with a larger S(j). These results suggest that cortical taste neurons differentially contribute to the coding of taste qualities. Input neurons with a larger S(j) tended to be with a larger variation of neural discharge rates to the basic taste stimuli. The variation of neural discharges may be important in the coding of taste qualities.

Algorithms↗
PubMed1997

Mice with a targeted disruption of the neurotrophin receptor trkB lose their gustatory ganglion cells early but do develop taste buds.

The alleged ability of taste afferents to induce taste buds in developing animals is investigated using a mouse model with a targeted deletion of the tyrosine kinase receptor trkB for the neurotrophin BDNF. This neurotrophin was recently shown to be expressed in developing taste buds and the receptor trkB has been shown to be expressed in the developing ganglion cells that innervate the taste buds. Our data show a reduction of geniculate ganglion cells to about 5% of control animals in neonates. Degeneration of ganglion cells starts when processes reach the central target (solitary tract) but before they reach the peripheral target (taste buds). Degeneration of ganglion cells is almost completed in trkB knockout mice before taste afferents reach in control animals the developing fungiform papillae. Four days later the first taste buds can be identified in fungiform papillae of both control and trkB knockout mice in about equal number and density. Many taste buds undergo a normal maturation compared to control animals. However, the more lateral and caudal fungiform papillae grow less in size and become less conspicuous in older trkB knockout mice. No intragemmal innervation can be found in trkB knockout taste buds but a few extragemmal fibers enter the apex and end between taste had cells without forming specialized synapses. Taste buds of trkB knockout mice appear less well organized than those of control mice, but some cells show similar vesicle accumulations as control taste bud cells in their base but no synaptic contact to an afferent. These data strongly suggest that the initial-development of many fungiform papillae and taste buds is independent of the specific taste innervation. It remains to be shown why others appear to be more dependent on proper innervation.

Animals↗
PubMed2006

Molecular definition of the taste of roasted cocoa nibs (Theobroma cacao) by means of quantitative studies and sensory experiments.

Sensory-guided decomposition of roasted cocoa nibs revealed that, besides theobromine and caffeine, a series of bitter-tasting 2,5-diketopiperazines and flavan-3-ols were the key inducers of the bitter taste as well as the astringent mouthfeel imparted upon consumption of roasted cocoa. In addition, a number of polyphenol glycopyranosides as well as a series of N-phenylpropenoyl-l-amino acids have been identified as key astringent compounds of roasted cocoa. In the present investigation, a total of 84 putative taste compounds were quantified in roasted cocoa beans and then rated for the taste contribution on the basis of dose-over-threshold (DoT) factors to bridge the gap between pure structural chemistry and human taste perception. To verify these quantitative results, an aqueous taste reconstitute was prepared by blending aqueous solutions of the individual taste compounds in their "natural" concentrations. Sensory analyses revealed that the taste profile of this artificial cocktail was very close to the taste profile of an aqueous suspension of roasted cocoa nibs. To further narrow down the number of key taste compounds, finally, taste omission experiments and human dose/response functions were performed, demonstrating that the bitter-tasting alkaloids theobromine and caffeine, seven bitter-tasting diketopiperazines, seven bitter- and astringent-tasting flavan-3-ols, six puckering astringent N-phenylpropenoyl-l-amino acids, four velvety astringent flavonol glycosides, gamma-aminobutyric acid, beta-aminoisobutyric acid, and six organic acids are the key organoleptics of the roasted cocoa nibs.

Cacao↗