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Burning Mouth Syndrome (BMS) presents as a persistent, often perplexing pain condition characterised primarily by a sensation of burning, yet frequently lacks observable clinical evidence. The underlying mechanisms of BMS remain elusive. Typically, the tongue bears the brunt of the discomfort, followed by the inner lower lip and hard palate. Psychologically, BMS often intersects with anxiety and depression, forming common comorbidities. There's emerging research suggesting a potential link between Human Herpesvirus 6B (HHV-6B) and mental health disorders. This association raises the possibility of HHV-6B as a contributor to BMS. HHV-6B's hypothesised involvement in BMS could be from various avenues: direct damage to taste cells and nerves, eliciting an inflammatory response, or even disrupting olfactory functions. This narrative review aims to critically evaluate the current literature on the potential association between HHV-6B and BMS. It explores the role of HHV-6B in pain mechanisms, inflammatory responses, and its impact on sensory functions such as taste and olfaction, providing a comprehensive overview of its implications in BMS pathogenesis. [ABSTRACT FROM AUTHOR]

Background and aims: Saliva is essential for the proper dilution and distribution of taste molecules on the tongue. It harbors extracellular vesicles (EVs), which mediate cell–cell communication. Changes in the composition of salivary EVs may arise under obese conditions and may potentially be involved in taste sensation and dysregulated eating behavior. Therefore, this study addresses the relationship between the size and concentration of salivary EVs and metabolic shifts in obesity or factors of taste sensation. Materials and methods: A total of 119 participants in the Obese Taste Bud (OTB) Study were included, who performed a standardized taste test, underwent taste bud density assessment, and were phenotypically characterized for anthropometrics, blood- and saliva adipokine levels, and various metabolic factors. Utilizing size exclusion chromatography followed by ultrafiltration, EVs were extracted from 2 mL of actively secreted saliva. EVs were characterized using nanoparticle tracking analyses, Western blot, and scanning transmission electron microscopy. Finally, group comparisons and bivariate correlation analyses were conducted. Results: Among the total cohort, the median size of salivary EVs was 190.05 nm, and the overall concentration ranged from 1.4 × 107 to 1.76 × 109 per mL of saliva. The size range and concentration of EVs per mL are negatively correlated (p = 0.0002, r = −0.264). Comparing lean participants (mean rank of 45.98) with those presenting obesity (mean rank of 34.46), a significant difference in the salivary EV content was observed (p = 0.029). Body weight, BMI, arm and calf circumferences, as well as the percentage of body fat were all negatively related to the concentration of EVs in all study participants (all p < 0.05, r > −0.2). No associations were found between the EV parameters and taste perception but serum alkaline phosphatase levels were negatively correlated (p = 0.007, r = −0.284) and adiponectin serum levels were positively correlated to the EV concentration (p = 0.036, r = 0.208). Conclusion: The current study provides evidence for the relation between salivary EVs and anthropometric as well as metabolic parameters of obesity. This can provide the basis for further research on the cargo of salivary EVs and how they may influence taste sensation, and may elucidate their potential connection to altered eating habits in obesity. [ABSTRACT FROM AUTHOR]

This study examined the anatomical and histological features of lingual papillae in squirrels. Two adult male squirrel tongues were used as the material in the study. Three parts were detected in the tongue: apex, corpus, and radix. There was a median sulcus on the apex of the tongue and an intermolar prominence on the body of the tongue. Five types of papillae such as filiform, conical, fungiform, vallate, and foliate were observed on the tongues of the squirrels. Filiform papillae were located from the apex of the tongue to the root as the dominant papilla. Conical papillae were observed on the intermolar prominence, on the sides of the tongue root, and between the vallate papillae. The direction of this papillae was oriented caudomedially. Fungiform papillae were randomly distributed among the filiform papillae. These papillae were mushroom shaped and had slits that separated them from filiform papillae. Three vallata papillae, arranged in a triangle with the apex pointing backward, were found on the root of the tongue. These papillae were surrounded by a trench. Foliate papillae were observed like mucosal folds in the caudolateral part of the tongue. On light microscopic examination, lingual papillae were covered with stratified squamous epithelium and had connective tissues. There were varying degrees of keratinization on the epithelial surfaces of the papillae. Although taste buds were seen in the epithelial layer of the fungiform and vallate papillae, they were not observed in the epithelium of the grooves of the foliate papillae. The findings obtained in the study were compared with those obtained from the lingual papillae of other rodents, and similarities and differences were revealed. Anatomske in histološke značilnosti jezičnih papil na jeziku pri veverici (Sciurus vulgaris) Izvleček: V tej študiji smo preučevali anatomske in histološke značilnosti jezičnih papil pri vevericah. V študiji smo uporabili dva jezika odraslih samcev veveric. Določili smo tri dele jezika: vrh, telo in koren. Na vrhnjem delu jezika je bila sredinska brazda, na telesu jezika pa medmolarna izboklina. Na jezikih veveric smo opazili pet vrst papil: nitaste, konične, gobaste, otočkaste in listaste. Nitaste papile so bile prevladujoče, prisotne od vrha do korena jezika. Konične papile so bile prisotne na intermolarnem izrastku, na straneh korena jezika in med otočkastimi papilami. Usmerjene so bile kavdomedialno. Gobaste papile so bile naključno razporejene med nitastimi papilami. Te papile so bile v obliki gobe z režami, ki so jih ločevale od filiformnih papil. Na korenu jezika so bile tri otočkaste papile razporejene v trikotnik z nazaj obrnjenim vrhom. Obdane so bile z jarkom. Listaste papile so bile v obliki gube sluznice v kavdolateralnem delu jezika. Pod svetlobnim mikroskopom so bile jezične papile pokrite z večskladnim ploščatim epitelijem, imele so vezivno tkivo. Na epitelijskih površinah papil so bile vidne različne stopnje poroženevanja. Čeprav so bile v epitelijski plasti gobastih in otočkastih papil vidne brbončice, jih v epiteliju žlebov listastih papil ni bilo opaziti. Ugotovitve, pridobljene v tej študiji, smo primerjali z ugotovitvami študij jezičnih papil drugih glodavcev ter prikazali podobnosti in razlike med njimi. Ključne besede: svetlobna mikroskopija; jezične papile; glodavec; veverica; brbončica

Background and aims: Saliva is essential for the proper dilution and distribution of taste molecules on the tongue. It harbors extracellular vesicles (EVs), which mediate cell–cell communication. Changes in the composition of salivary EVs may arise under obese conditions and may potentially be involved in taste sensation and dysregulated eating behavior. Therefore, this study addresses the relationship between the size and concentration of salivary EVs and metabolic shifts in obesity or factors of taste sensation. Materials and methods: A total of 119 participants in the Obese Taste Bud (OTB) Study were included, who performed a standardized taste test, underwent taste bud density assessment, and were phenotypically characterized for anthropometrics, blood- and saliva adipokine levels, and various metabolic factors. Utilizing size exclusion chromatography followed by ultrafiltration, EVs were extracted from 2 mL of actively secreted saliva. EVs were characterized using nanoparticle tracking analyses, Western blot, and scanning transmission electron microscopy. Finally, group comparisons and bivariate correlation analyses were conducted. Results: Among the total cohort, the median size of salivary EVs was 190.05 nm, and the overall concentration ranged from 1.4 × 107 to 1.76 × 109 per mL of saliva. The size range and concentration of EVs per mL are negatively correlated (p = 0.0002, r = −0.264). Comparing lean participants (mean rank of 45.98) with those presenting obesity (mean rank of 34.46), a significant difference in the salivary EV content was observed (p = 0.029). Body weight, BMI, arm and calf circumferences, as well as the percentage of body fat were all negatively related to the concentration of EVs in all study participants (all p < 0.05, r > −0.2). No associations were found between the EV parameters and taste perception but serum alkaline phosphatase levels were negatively correlated (p = 0.007, r = −0.284) and adiponectin serum levels were positively correlated to the EV concentration (p = 0.036, r = 0.208). Conclusion: The current study provides evidence for the relation between salivary EVs and anthropometric as well as metabolic parameters of obesity. This can provide the basis for further research on the cargo of salivary EVs and how they may influence taste sensation, and may elucidate their potential connection to altered eating habits in obesity.

A subset of gustatory cells are serotonin immunoreactive (ir) in the mammalian taste bud. In the taste bud of lamprey, elongated gustatory-like cells are also serotonin-ir. In contrast, flattened serotonin-ir cells are located only in the basal region of the taste buds in the teleosts and amphibians. These serotonin-ir cells are termed as basal cells. To evaluate the evolution and diversity of serotonergic cells in the taste bud of amniote animals, we explored the distribution and morphology of serotonin-ir cells in the taste buds of ancestral actinopterygian fish (spotted gar, sturgeon, Polypterus senegalus) and elasmobranch (stingray). In all examined animals, the taste buds contained serotonin-ir cells in their basal part. The number of serotonin-ir basal cells in each taste bud was different between these fish species. They were highest in the stingray and decreased in the order of the Polypterus, sturgeon, and gar. While serotonin immunoreactivity was observed only in the basal cells in the taste buds of the ancestral actinopterygian fish, some elongated cells were also serotonin-ir in addition to the basal cells in the stingray taste buds. mRNA of tryptophan hydroxylase 1 (tph1), a rate-limiting enzyme of the serotonin synthesis, is expressed in both the elongated and basal cells of stingray taste buds, indicating that these cells synthesize the serotonin by themselves. These results suggest that the serotonin-ir basal cells arose from the ancestor of the cartilaginous fish, and serotonin-ir cells in the elasmobranch taste bud exhibit an intermediate aspect between the lamprey and actinopterygian fish. [ABSTRACT FROM AUTHOR]

GPRC5C is an orphan G protein‐coupled receptor (GPCR) that belongs to the class C GPCR family. Although GPRC5C is expressed in various organs, its function and ligand are still undetermined. We found that GPRC5C is expressed in mouse taste cells, enterocytes, and pancreatic α‐cells. In functional imaging assays, HEK293 cells heterologously expressing GPRC5C and the chimeric G protein α subunit Gα16‐gust44 showed robust intracellular Ca2+ increases in response to monosaccharides, disaccharides, and a sugar alcohol, but not an artificial sweetener or sweet‐tasting amino acid. Notably, Ca2+ increases occurred after washout, not during stimulation. Our findings suggest that GPRC5C has receptor properties which lead to novel 'off' responses to saccharide detachment and may work as an internal or external chemosensor specifically tuned to natural sugars. [ABSTRACT FROM AUTHOR]

Mammalian taste bud cells are composed of several distinct cell types and differentiated from surrounding tongue epithelial cells. However, the detailed mechanisms underlying their differentiation have yet to be elucidated. In the present study, we examined an Ascl1-expressing cell lineage using circumvallate papillae (CVP) of newborn mice and taste organoids (three-dimensional self-organized tissue cultures), which allow studying the differentiation of taste bud cells in fine detail ex vivo. Using lineage-tracing analysis, we observed that Ascl1 lineage cells expressed type II and III taste cell markers both CVP of newborn mice and taste organoids. However, the coexpression rate in type II cells was lower than that in type III cells. Furthermore, we found that the generation of the cells which express type II and III cell markers was suppressed in taste organoids lacking Ascl1-expressing cells. These findings suggest that Ascl1-expressing precursor cells can differentiate into both type III and a subset of type II taste cells. [ABSTRACT FROM AUTHOR]

Taste ganglion neurons are functionally and molecularly diverse, but until recently morphological diversity was completely unexplored. Specifically, taste arbors (the portion of the neuron within the taste bud) vary in structure, but the reason for this variability is unclear. Here, we analyzed structural variability in taste arbors to determine which factors determine their morphological diversity. To characterize arbor morphology and its relationship to taste bud cells capable of transducing taste stimuli (taste‐transducing cell) number and type, we utilized sparse cell genetic labeling of taste ganglion neurons in combination with whole‐mount immunohistochemistry. Reconstruction of 151 taste arbors revealed variation in arbor size, complexity, and symmetry. Overall, taste arbors exist on a continuum of complexity, cannot be categorized into discrete morphological groups, and do not have stereotyped endings. Arbor size/complexity was not related to the size of the taste bud in which it was located or the type of taste‐transducing cell contacted (membranes within 180 nm). Instead, arbors could be broadly categorized into three groups: large asymmetrical arbors contacting many taste‐transducing cells, small symmetrical arbors contacting one or two taste‐transducing cells, and unbranched arbors. Neurons with multiple arbors had arbors in more than one of these categories, indicating that this variability is not an intrinsic feature of neuron type. Instead, we speculate that arbor structure is determined primarily by nerve fiber remodeling in response to cell turnover and that large asymmetrical arbors represent a particularly plastic state. [ABSTRACT FROM AUTHOR]

Sensory receptors across the entire tongue are engaged during eating. However, the tongue has distinctive regions with taste (fungiform and circumvallate) and non-taste (filiform) organs that are composed of specialized epithelia, connective tissues, and innervation. The tissue regions and papillae are adapted in form and function for taste and somatosensation associated with eating. It follows that homeostasis and regeneration of distinctive papillae and taste buds with particular functional roles require tailored molecular pathways. Nonetheless, in the chemosensory field, generalizations are often made between mechanisms that regulate anterior tongue fungiform and posterior circumvallate taste papillae, without a clear distinction that highlights the singular taste cell types and receptors in the papillae. We compare and contrast signaling regulation in the tongue and emphasize the Hedgehog pathway and antagonists as prime examples of signaling differences in anterior and posterior taste and non-taste papillae. Only with more attention to the roles and regulatory signals for different taste cells in distinct tongue regions can optimal treatments for taste dysfunctions be designed. In summary, if tissues are studied from one tongue region only, with associated specialized gustatory and non-gustatory organs, an incomplete and potentially misleading picture will emerge of how lingual sensory systems are involved in eating and altered in disease. [ABSTRACT FROM AUTHOR]

Taste buds on the tongue contain taste receptor cells (TRCs) that detect sweet, sour, salty, umami and bitter stimuli. Like non-taste lingual epithelium, TRCs are renewed frombasal keratinocytes, many of which express the transcription factor SOX2. Genetic lineage tracing has shown that SOX2+ lingual progenitors give rise to both taste and non-taste lingual epithelium in the posterior circumvallate taste papilla (CVP) of mice. However, SOX2 is variably expressed among CVP epithelial cells, suggesting that their progenitor potential may vary. Using transcriptome analysis and organoid technology, we show that cells expressing SOX2 at higher levels are taste-competent progenitors that give rise to organoids comprising both TRCs and lingual epithelium. Conversely, organoids derived from progenitors that express SOX2 at lower levels are composed entirely of non-taste cells. Hedgehog and WNT/ß-catenin are required for taste homeostasis in adult mice. However, manipulation of hedgehog signaling in organoids has no impact on TRC differentiation or progenitor proliferation. By contrast, WNT/ß-catenin promotes TRC differentiation in vitro in organoids derived from higher but not low SOX2+ expressing progenitors. [ABSTRACT FROM AUTHOR]

Members of the Eya family, which are a class of transcription factors with phosphatase activity, are widely expressed in cranial sensory organs during development. However, it is unclear whether these genes are expressed in the taste system during development and whether they play any role in specifying taste cell fate. In this study, we report that Eya1 is not expressed during embryonic tongue development but that Eya1-expressing progenitors in somites or pharyngeal endoderm give rise to tongue musculature or taste organs, respectively. In the Eya1-deficient tongues, these progenitors do not proliferate properly, resulting in a smaller tongue at birth, impaired growth of taste papillae, and disrupted expression of Six1 in the papillary epithelium. On the other hand, Eya2 is specifically expressed in endoderm-derived circumvallate and foliate papillae located on the posterior tongue during development. In adult tongues, Eya1 is predominantly expressed in IP3R3-positive taste cells in the taste buds of the circumvallate and foliate papillae, while Eya2 is persistently expressed in these papillae at higher levels in some epithelial progenitors and at lower levels in some taste cells. We found that conditional knockout of Eya1 in the third week or Eya2 knockout reduced Pou2f3+, Six1+ and IP3R3+ taste cells. Our data define for the first time the expression patterns of Eya1 and Eya2 during the development and maintenance of the mouse taste system and suggest that Eya1 and Eya2 may act together to promote lineage commitment of taste cell subtypes.

Taste sensation is the process of converting chemical identities in food into a neural code of the brain. Taste information is initially formed in the taste buds on the tongue, travels through the afferent gustatory nerves to the sensory ganglion neurons, and finally reaches the multiple taste centers of the brain. In the taste field, optical tools to observe cellularlevel functions play a pivotal role in understanding how taste information is processed along a pathway. In this review, we introduce recent advances in the optical tools used to study the taste transduction pathways. [ABSTRACT FROM AUTHOR]

The neural basis of tongue mechanosensation remains largely mysterious despite the tongue's high tactile acuity, sensitivity, and relevance to ethologically important functions. We studied terminal morphologies and tactile responses of lingual afferents from the trigeminal ganglion. Fungiform papillae, the taste-bud-holding structures in the tongue, were convergently innervated by multiple Piezo2+ trigeminal afferents, whereas single trigeminal afferents branched into multiple adjacent filiform papillae. In vivo single-unit recordings from the trigeminal ganglion revealed lingual low-threshold mechanoreceptors (LTMRs) with distinct tactile properties ranging from intermediately adapting (IA) to rapidly adapting (RA). The receptive fields of these LTMRs were mostly less than 0.1 mm2 and concentrated at the tip of the tongue, resembling the distribution of fungiform papillae. Our results indicate that fungiform papillae are mechanosensory structures and suggest a simple model that links functional and anatomical properties of tactile sensory neurons in the tongue. [Display omitted] • The tip of the tongue is heavily innervated by lingual mechanoreceptors • Lingual LTMRs have small receptive fields and high sensitivity and adapt rapidly • Lingual afferents exhibit distinct innervation patterns in different papilla types • Fungiform papillae, the lingual papillae containing taste buds, are touch sensors The tip of the tongue, one of the most tactile-sensitive areas in the body, is enriched with taste-bud-containing fungiform papillae. Zhang et al. reveal that fungiform papillae are touch sensors and suggest a model linking functional and anatomical properties of tactile sensory neurons in the tongue. [ABSTRACT FROM AUTHOR]

Zinc is an essential trace element, and its deficiency causes taste dysfunction. Zinc accumulates in zinc transporter (ZnT)3-expressing presynaptic vesicles in hippocampal neurons and acts as a neurotransmitter in the central nervous system. However, the distribution of zinc and its role as a signal transmitter in taste buds remain unknown. Therefore, we examined the distribution of zinc and expression profiles of ZnT3 in taste cells and evaluated zinc release from isolated taste cells upon taste stimuli. Taste cells with a spindle or pyriform morphology were revealed by staining with the fluorescent zinc dye ZnAF-2DA and autometallography in the taste buds of rat circumvallate papillae. Znt3 mRNA levels were detected in isolated taste buds. ZnT3-immunoreactivity was found in phospholipase-β2-immunopositive type II taste cells and aromatic amino acid decarboxylase-immunopositive type III cells but not in nucleoside triphosphate diphosphohydrolase 2-immunopositive type I cells. Moreover, we examined zinc release from taste cells using human transient receptor potential A1-overexpressing HEK293 as zinc-sensor cells. These cells exhibited a clear response to isolated taste cells exposed to taste stimuli. However, pretreatment with magnesium-ethylenediaminetetraacetic acid, an extracellular zinc chelator - but not with zinc-ethylenediaminetetraacetic acid, used as a negative control - significantly decreased the response ratio of zinc-sensor cells. These findings suggest that taste cells release zinc to the intercellular area in response to taste stimuli and that zinc may affect signaling within taste buds.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections cause loss or alteration of taste and smell as early symptoms and sequelae, but the detailed mechanism remains unclear. This study investigated whether coronavirus disease 2019-induced taste disorders are caused by direct effects on taste bud cells. SARS-CoV-2 recombinant spike and nucleocapsid proteins were applied to circumvallate papillae of male Sprague–Dawley rats. Immunohistochemistry and image analysis were used to compare the number of taste buds, and taste bud cells and area, together with confirmation of angiotensin-converting enzyme 2 (ACE2) expression. Immunohistochemical analysis revealed ACE2 expression in the taste buds of rat circumvallate papillae. Decreases in the number of taste buds, taste bud cells, and their area were observed at 12 days after application of SARS-CoV-2 recombinant spike and nucleocapsid proteins. These data suggest that SARS-CoV-2 proteins induce degeneration of taste buds. [ABSTRACT FROM AUTHOR]

Background: Hedgehog (HH) signaling is essential for homeostasis in gustatory fungiform papillae (FP) and taste buds. However, activities of HH antagonists in these tissues remain unexplored. We investigated a potential role for HH‐interacting protein (HHIP), an endogenous pathway antagonist, in regulating HH signaling during taste organ homeostasis. We found a restricted pattern of Hhip‐expressing cells in the anterior epithelium of each nongustatory filiform papilla (FILIF) only. To test for roles in antagonism of HH signaling, we investigated HHIP after pathway inhibition with SMO inhibition via sonidegib and Smo deletion, Gli2 deletion/suppression, or with chorda tympani/lingual nerve cut. Results: In all approaches, the HHIP expression pattern was retained in FILIF suggesting HH‐independent regulation of HHIP. Remarkably, after pathway inhibition, HHIP expression was detected also in the conical, FILIF‐like atypical FP. We found a close association of de novo expression of HHIP in atypical FP with loss of Gli1+, HH‐responding cells. Further, we report that PTCH1 is another potential HH antagonist in FILIF that co‐localizes with HHIP. Conclusions: After HH pathway inhibition the ectopic expression of HHIP correlates with a FILIF‐like morphology in atypical FP and we propose that localized expression of the HH antagonist HHIP regulates pathway inhibition to maintain FILIF during tongue homeostasis. Key Findings: Unique and restricted expression of Hedgehog antagonist, HHIP in filiform papillae.Ectopic HHIP expression after Hedgehog signaling inhibition.Cell type‐specific regulation of core Hedgehog pathway components in the adult tongue.Ptch1 emerged to have dual role: Hedgehog receptor in fungiform papillae and Hedgehog antagonist in filiform papillae. [ABSTRACT FROM AUTHOR]

The biological taste system has the unique ability to detect taste substances. Biomaterials originating from a biological taste system have been recognized as ideal candidates to serve as sensitive elements in the development of taste-based biosensors. In this study, we developed a taste bud organoid-based biosensor for the research of taste sensation. Taste bud organoids prepared from newborn mice were cultured and loaded onto the surface of a 64-channel microelectrode array (MEA) chip to explore the electrophysiological changes upon taste; an MEA chip was used to simultaneously record multiple-neuron firing activities from taste bud organoids under different taste stimuli, which helped to reveal the role of taste buds in taste sensing. The obtained results show that taste cells separated from the taste epithelium grew well into spherical structures under 3D culture conditions. These structures were composed of multiple cells with obvious budding structures. Moreover, the multicellular spheres were seeded on a 64-channel microelectrode array and processed with different taste stimuli. It was indicated that the MEA chip could efficiently monitor the electrophysiological signals from taste bud organoids in response to various taste stimuli. This biosensor provides a new method for the study of taste sensations and taste bud functions. [ABSTRACT FROM AUTHOR]

Sensory receptors across the entire tongue are engaged during eating. However, the tongue has distinctive regions with taste (fungiform and circumvallate) and non-taste (filiform) organs that are composed of specialized epithelia, connective tissues, and innervation. The tissue regions and papillae are adapted in form and function for taste and somatosensation associated with eating. It follows that homeostasis and regeneration of distinctive papillae and taste buds with particular functional roles require tailored molecular pathways. Nonetheless, in the chemosensory field, generalizations are often made between mechanisms that regulate anterior tongue fungiform and posterior circumvallate taste papillae, without a clear distinction that highlights the singular taste cell types and receptors in the papillae. We compare and contrast signaling regulation in the tongue and emphasize the Hedgehog pathway and antagonists as prime examples of signaling differences in anterior and posterior taste and non-taste papillae. Only with more attention to the roles and regulatory signals for different taste cells in distinct tongue regions can optimal treatments for taste dysfunctions be designed. In summary, if tissues are studied from one tongue region only, with associated specialized gustatory and non-gustatory organs, an incomplete and potentially misleading picture will emerge of how lingual sensory systems are involved in eating and altered in disease.

Sensory cells that specialize in transducing olfactory and gustatory stimuli are renewed throughout life and can regenerate after injury unlike their counterparts in the mammalian retina and auditory epithelium. This uncommon capacity for regeneration offers an opportunity to understand mechanisms that promote the recovery of sensory function after taste and smell loss. Immune responses appear to influence degeneration and later regeneration of olfactory sensory neurons and taste receptor cells. Here we review surgical, chemical, and inflammatory injury models and evidence that immune responses promote or deter chemosensory cell regeneration. Macrophage and neutrophil responses to chemosensory receptor injury have been the most widely studied without consensus on their net effects on regeneration. We discuss possible technical and biological reasons for the discrepancy, such as the difference between peripheral and central structures, and suggest directions for progress in understanding immune regulation of chemosensory regeneration. Our mechanistic understanding of immune-chemosensory cell interactions must be expanded before therapies can be developed for recovering the sensation of taste and smell after head injury from traumatic nerve damage and infection. Chemosensory loss leads to decreased quality of life, depression, nutritional challenges, and exposure to environmental dangers highlighting the need for further studies in this area. [ABSTRACT FROM AUTHOR]

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Key points: Taste transduction occurs in taste buds in the tongue epithelium.The Ca2+‐activated Cl– channels TMEM16A and TMEM16B play relevant physiological roles in several sensory systems.Here, we report that TMEM16A, but not TMEM16B, is expressed in the apical part of taste buds.Large Ca2+‐activated Cl− currents blocked by Ani‐9, a selective inhibitor of TMEM16A, are measured in type I taste cells but not in type II or III taste cells.ATP indirectly activates Ca2+‐activated Cl– currents in type I cells through TMEM16A channels.These results indicate that TMEM16A is functional in type I taste cells and contribute to understanding the largely unknown physiological roles of these cells. The Ca2+‐activated Cl– channels TMEM16A and TMEM16B have relevant roles in many physiological processes including neuronal excitability and regulation of Cl– homeostasis. Here, we examined the presence of Ca2+‐activated Cl– channels in taste cells of mouse vallate papillae by using immunohistochemistry and electrophysiological recordings. By using immunohistochemistry we showed that only TMEM16A, and not TMEM16B, was expressed in taste bud cells where it largely co‐localized with the inwardly rectifying K+ channel KNCJ1 in the apical part of type I cells. By using whole‐cell patch‐clamp recordings in isolated cells from taste buds, we measured an average current of −1083 pA at −100 mV in 1.5 μm Ca2+ and symmetrical Cl– in type I cells. Ion substitution experiments and blockage by Ani‐9, a specific TMEM16A channel blocker, indicated that Ca2+ activated anionic currents through TMEM16A channels. We did not detect any Ca2+‐activated Cl– currents in type II or III taste cells. ATP is released by type II cells in response to various tastants and reaches type I cells where it is hydrolysed by ecto‐ATPases. Type I cells also express P2Y purinergic receptors and stimulation of type I cells with extracellular ATP produced large Ca2+‐activated Cl− currents blocked by Ani‐9, indicating a possible role of TMEM16A in ATP‐mediated signalling. These results provide a definitive demonstration that TMEM16A‐mediated currents are functional in type I taste cells and provide a foundation for future studies investigating physiological roles for these often‐neglected taste cells. Key points: Taste transduction occurs in taste buds in the tongue epithelium.The Ca2+‐activated Cl– channels TMEM16A and TMEM16B play relevant physiological roles in several sensory systems.Here, we report that TMEM16A, but not TMEM16B, is expressed in the apical part of taste buds.Large Ca2+‐activated Cl− currents blocked by Ani‐9, a selective inhibitor of TMEM16A, are measured in type I taste cells but not in type II or III taste cells.ATP indirectly activates Ca2+‐activated Cl– currents in type I cells through TMEM16A channels.These results indicate that TMEM16A is functional in type I taste cells and contribute to understanding the largely unknown physiological roles of these cells. [ABSTRACT FROM AUTHOR]

ABSTRACT: Chickens have been reported to have a low taste bud count and thus low taste acuity. However, more recent studies indicate that the earlier reported count of chicken taste buds may have been significantly underestimated. To answer the question of whether the taste sensing system in broiler chickens evolved during the breeding selection over the past decades, we compared the taste sensitivity to bitter and taste buds between a meat-type control strain – the 1955 Athens Canadian Random Bred (ACRB), and a modern high-yielding broiler strain – the 2012 Cobb 500. The behavioral tests showed that the ACRB did not avoid bitter taste solutions of quinine hydrochloride (QHCl) at the examined concentrations (0.5, 1, 2, and 4 mM) (P > 0.05), while the Cobb 500 significantly avoided both the 2 mM and 4 mM QHCl solutions (P < 0.01). The labeling of chicken taste buds using the molecular marker Vimentin revealed that Cobb 500 chickens had a slightly higher number (P < 0.1), but lower density of taste bud clusters in the palate (P < 0.01) and the base of the oral cavity (P < 0.05) compared to the ACRB. We also found that a single amino acid change occurred in the bitter taste receptor T2R7. However, the functional analyses using HEK293T cells transiently expressing T2R7 revealed that the functions of T2R7 were comparable between the two strains. Taken together, our results demonstrated that taste sensitivities could be affected by the selection of the broiler chickens. The modern high-yielding broilers, which have massive feed intake and appetite, had a higher sensitivity to bitter taste stimuli than the meat-type chicken strain which was established decades ago. This evolvement of taste sensitivities may be associated with the alterations of an upper level of taste system, rather than the peripheral taste system, including distribution of taste buds and functions of taste receptors.

Embryonic taste bud primordia are specified as taste placodes on the tongue surface and differentiate into the first taste receptor cells (TRCs) at birth. Throughout adult life, TRCs are continually regenerated from epithelial progenitors. Sonic hedgehog (SHH) signaling regulates TRC development and renewal, repressing taste fate embryonically, but promoting TRC differentiation in adults. Here, using mouse models, we show TRC renewal initiates at birth and coincides with onset of SHHs pro-taste function. Using transcriptional profiling to explore molecular regulators of renewal, we identified Foxa1 and Foxa2 as potential SHH target genes in lingual progenitors at birth and show that SHH overexpression in vivo alters FoxA1 and FoxA2 expression relevant to taste buds. We further bioinformatically identify genes relevant to cell adhesion and cell locomotion likely regulated by FOXA1;FOXA2 and show that expression of these candidates is also altered by forced SHH expression. We present a new model where SHH promotes TRC differentiation by regulating changes in epithelial cell adhesion and migration.

The biological taste system has the unique ability to detect taste substances. Biomaterials originating from a biological taste system have been recognized as ideal candidates to serve as sensitive elements in the development of taste-based biosensors. In this study, we developed a taste bud organoid-based biosensor for the research of taste sensation. Taste bud organoids prepared from newborn mice were cultured and loaded onto the surface of a 64-channel microelectrode array (MEA) chip to explore the electrophysiological changes upon taste; an MEA chip was used to simultaneously record multiple-neuron firing activities from taste bud organoids under different taste stimuli, which helped to reveal the role of taste buds in taste sensing. The obtained results show that taste cells separated from the taste epithelium grew well into spherical structures under 3D culture conditions. These structures were composed of multiple cells with obvious budding structures. Moreover, the multicellular spheres were seeded on a 64-channel microelectrode array and processed with different taste stimuli. It was indicated that the MEA chip could efficiently monitor the electrophysiological signals from taste bud organoids in response to various taste stimuli. This biosensor provides a new method for the study of taste sensations and taste bud functions.

Circumvallate papilla (CVP) is a distinctively structured with dome-shaped apex, and the surrounding trench which contains over two hundred taste buds on the lateral walls. Although CVP was extensively studied to determine the regulatory mechanisms during organogenesis, it still remains to be elucidated the principle mechanisms of signaling regulations on morphogenesis including taste buds formation. The key role of Yes-associated protein (YAP) in the regulation of organ size and cell proliferation in vertebrates is well understood, but little is known about the role of this signaling pathway in CVP development. We aimed to determine the putative roles of YAP signaling in the epithelial patterning during CVP morphogenesis. To evaluate the precise localization patterns of YAP and other related signaling molecules, including β-catenin, Ki67, cytokeratins, and PGP9.5, in CVP tissue, histology and immunohistochemistry were employed at E16 and adult mice. Our results suggested that there are specific localization patterns of YAP and Wnt signaling molecules in developing and adult CVP. These concrete localization patterns would provide putative involvements of YAP and Wnt signaling for proper epithelial cell differentiation including the formation and maintenance of taste buds. [ABSTRACT FROM AUTHOR]

Mammalian taste bud cells have a limited lifespan and differentiate into type I, II, and III cells from basal cells (type IV cells) (postmitotic precursor cells). However, little is known regarding the cell lineage within taste buds. In this study, we investigated the cell fate of Mash1-positive precursor cells utilizing the Cre-loxP system to explore the differentiation of taste bud cells. We found that Mash1-expressing cells in Ascl1CreERT2::CAG-floxed tdTomato mice differentiated into taste bud cells that expressed aromatic L-amino acid decarboxylase (AADC) and carbonic anhydrase IV (CA4) (type III cell markers), but did not differentiate into most of gustducin (type II cell marker)-positive cells. Additionally, we found that Mash1-expressing cells could differentiate into phospholipase C β2 (PLCβ2)-positive cells, which have a shorter lifespan compared with AADC- and CA4-positive cells. These results suggest that Mash1-positive precursor cells could differentiate into type III cells, but not into most of type II cells, in the taste buds. [ABSTRACT FROM AUTHOR]

Heterotrimeric G protein-coupled receptors (GPCRs) comprise the largest receptor family in mammals and are responsible for the regulation of most physiological functions. Besides mediating the sensory modalities of olfaction and vision, GPCRs also transduce signals for three basic taste qualities of sweet, umami (savory taste), and bitter, as well as the flavor sensation kokumi. Taste GPCRs reside in specialised taste receptor cells (TRCs) within taste buds. Type I taste GPCRs (TAS1R) form heterodimeric complexes that function as sweet (TAS1R2/TAS1R3) or umami (TAS1R1/TAS1R3) taste receptors, whereas Type II are monomeric bitter taste receptors or kokumi/calcium-sensing receptors. Sweet, umami and kokumi receptors share structural similarities in containing multiple agonist binding sites with pronounced selectivity while most bitter receptors contain a single binding site that is broadly tuned to a diverse array of bitter ligands in a non-selective manner. Tastant binding to the receptor activates downstream secondary messenger pathways leading to depolarization and increased intracellular calcium in TRCs, that in turn innervate the gustatory cortex in the brain. Despite recent advances in our understanding of the relationship between agonist binding and the conformational changes required for receptor activation, several major challenges and questions remain in taste GPCR biology that are discussed in the present review. In recent years, intensive integrative approaches combining heterologous expression, mutagenesis and homology modeling have together provided insight regarding agonist binding site locations and molecular mechanisms of orthosteric and allosteric modulation. In addition, studies based on transgenic mice, utilizing either global or conditional knock out strategies have provided insights to taste receptor signal transduction mechanisms and their roles in physiology. However, the need for more functional studies in a physiological context is apparent and would be enhanced by a crystallized structure of taste receptors for a more complete picture of their pharmacological mechanisms.

The electron microscopic and histological studies of the buccal‐cavity of herbivorous fish Mola (Amblypharyngodon mola) were performed. The studies revealed that the architectures of the buccal cavity of A. mola support the herbivory nature of the fish. Both the upper and lower jaws of the fish are rich in mucus glands, unculi, and microridges. The presence of papillae like taste buds in the lower jaw of A. mola indicates the mechanosensory role of the lower jaw during gustation. These features directly support a gustatory feeding behavior associated with filter feeding in this small freshwater fish. [ABSTRACT FROM AUTHOR]

In the last few years, single-cell profiling of taste cells and ganglion cells has advanced our understanding of transduction, encoding, and transmission of information from taste buds as relayed to the central nervous system. This review focuses on new knowledge from these molecular approaches and attempts to place this in the context of previous questions and findings in the field. The individual taste cells within a taste bud are molecularly specialized for detection of one of the primary taste qualities: salt, sour, sweet, umami, and bitter. Transduction and transmitter release mechanisms differ substantially for taste cells transducing sour (Type III cells) compared with those transducing the qualities of sweet, umami, or bitter (Type II cells), although ultimately all transmission of taste relies on activation of purinergic P2X receptors on the afferent nerves. The ganglion cells providing innervation to the taste buds also appear divisible into functional and molecular subtypes, and each ganglion cell is primarily but not exclusively responsive to one taste quality.

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In clinical orthodontic treatment, chronic respiratory disturbance or mouth breathing has been concerned symptoms and screening criteria. In this study, to analyze the relation between nasal obstruction and taste sensing, a unilateral nasal obstruction model was performed to investigate the taste papillae and taste buds in rats. Methods: Fourteen 6-day-old male Wistar rats were randomly divided into control and experimental groups (n = 7 each). The experimental group underwent unilateral nasal obstruction at 8 days of age. The rats were euthanized at 9-week-old. The morphology of the circumvallate papillae and taste buds were identified by immunohistochemical methods. The fungiform papillae were visualized with 1% methylene blue and sectioned for taste bud observation. Results: Some defects in the gustatory epithelium were observed after unilateral nasal obstruction. Rats in the experimental group had significantly fewer fungiform papillae and smaller volumes of taste bud. In circumvallate papillae, smaller total taste bud area was found in experiment group. Conclusion: Findings in the present study suggest that nasal obstruction might have significant influences on the gustatory function via morphologic change in the taste papillae and taste buds in tongue area.

Exposure of the oral cavity to acidic solutions evokes not only a sensation of sour, but also of sharp or tangy. Acidic substances potentially stimulate both taste buds and acid-sensitive mucosal free nerve endings. Mice lacking taste function (P2X2/P2X3 double-KO mice) refuse acidic solutions similar to wildtype (WT) mice and intraoral infusion of acidic solutions in these KO animals evokes substantial c-Fos activity within orosensory trigeminal nuclei as well as of the nucleus of the solitary tract (nTS) (Stratford, Thompson, et al. 2017). This residual acid-evoked, non-taste activity includes areas that receive inputs from trigeminal and glossopharyngeal peptidergic (CGRP-containing) nerve fibers that express TrpA1 and TrpV1 both of which are activated by low pH. We compared avoidance responses in WT and TrpA1/V1 double-KO (TRPA1/V1Dbl−/−) mice in brief-access behavioral assay (lickometer) to 1, 3, 10, and 30 mM citric acid, along with 100 µM SC45647 and H2O. Both WT and TRPA1/V1Dbl−/− show similar avoidance, including to higher concentrations of citric acid (10 and 30 mM; pH 2.62 and pH 2.36, respectively), indicating that neither TrpA1 nor TrpV1 is necessary for the acid-avoidance behavior in animals with an intact taste system. Similarly, induction of c-Fos in the nTS and dorsomedial spinal trigeminal nucleus was similar in the WT and TRPA1/V1Dbl−/− animals. Taken together these results suggest non-TrpV1 and non-TrpA1 receptors underlie the residual responses to acids in mice lacking taste function. [ABSTRACT FROM AUTHOR]

The Florida manatee, Trichechus manatus latirostris, is a fully aquatic, threatened marine mammal for which increased understanding of their physiology, reproduction, and nutrition supports management decisions. Manatees may use taste to distinguish saltwater gradients, toxin detection, food assessment, and social interactions. This study sought to locate and characterize manatee taste buds comparing location, structure, number, and size to other species. Entire heads from manatees (6 males, 4 females) of various ages were obtained. The muzzle, tissue surrounding the nares, oral cavity, and epiglottis were examined grossly for pits and papillae. Tissues were examined using light and transmission electron microscopy. Within the predominant taste bud location, the tongue root, taste bud number was estimated using samples from four animals. The average number of taste buds within the tongue root was 11,534 (range 2,711–23,237) with sparse taste buds located on the soft palate and epiglottis. The location along the lateral surface of the tongue root and bordered by grooves, through which tastants could be easily transported, has functional significance. Large numbers of taste buds within the tongue root suggest that taste is an important component of manatee sensory systems and behavioral research would clarify this. [ABSTRACT FROM AUTHOR]

Inflammatory cytokines are signaling molecules that regulate numerous physiological processes, from tissue homeostasis to metabolism and food intake. Expression of certain cytokines can be markedly induced in subsets of taste bud cells under acute and chronic inflammation. This may contribute to altered taste perception and preference associated with many diseases. Although the pathways of cytokine induction are well studied in immune cells, they remain poorly characterized in taste cells, in part due to the difficulties of performing biochemical analyses with a limited number of taste cells. The recently developed taste organoid model provides an opportunity to carry out these mechanistic studies in vitro. However, it was unknown whether taste organoids respond to inflammatory stimuli as do in vivo native taste buds. Here we analyze lipopolysaccharide (LPS)-induced expression and secretion of two inflammatory cytokines, tumor necrosis factor (TNF), and interleukin-6 (IL-6). We show that, similarly to native mouse taste epithelia, organoids derived from mouse circumvallate stem cells express several toll-like receptors (TLRs), including TLR4—the primary receptor for LPS. Organoids and native taste epithelia express all five genes in the nuclear factor-κb (Nfkb) family that encode the transcription factor NF-κB, a critical regulator of inflammatory responses. LPS stimulates fast induction of TNF and IL-6 with similar induction kinetics in organoids and native taste epithelia. These results show that taste epithelial cells possess necessary components for inflammatory cytokine induction and secretion and suggest that the organoid model can be a useful tool to dissect the underlying mechanisms. [ABSTRACT FROM AUTHOR]

The regenerative capacity of many placode-derived epithelial structures makes them of interest for understanding the molecular control of epithelial stem cells and their niches. Here, we investigate the interaction between the developing epithelium and its surrounding mesenchyme in one such system, the taste papillae and sensory taste buds of the mouse tongue. We identify follistatin (FST) as a mesenchymal factor that controls size, patterning and gustatory cell differentiation in developing taste papillae. FST limits expansion and differentiation of Sox2-expressing taste progenitor cells and negatively regulates the development of taste papillae in the lingual epithelium: in Fst(-/-) tongue, there is both ectopic development of Sox2-expressing taste progenitors and accelerated differentiation of gustatory cells. Loss of Fst leads to elevated activity and increased expression of epithelial Bmp7; the latter effect is consistent with BMP7 positive autoregulation, a phenomenon we demonstrate directly. We show that FST and BMP7 influence the activity and expression of other signaling systems that play important roles in the development of taste papillae and taste buds. In addition, using computational modeling, we show how aberrations in taste papillae patterning in Fst(-/-) mice could result from disruption of an FST-BMP7 regulatory circuit that normally suppresses noise in a process based on diffusion-driven instability. Because inactivation of Bmp7 rescues many of the defects observed in Fst(-/-) tongue, we conclude that interactions between mesenchyme-derived FST and epithelial BMP7 play a central role in the morphogenesis, innervation and maintenance of taste buds and their stem/progenitor cells.

Background: Multicellular taste buds located within taste papillae on the tongue mediate taste sensation. In taste papillae, taste bud cells (TBCs), such as taste receptor cells and taste precursor cells, and the surrounding lingual epithelium including epithelial progenitors (also called taste stem/progenitor cells) are maintained by continuous cell turnover throughout life. However, it remains unknown how the cells constituting taste buds proliferate and differentiate to maintain taste bud tissue. Based on in situ hybridization (ISH) screening, we demonstrated that the oncofetal antigen 5T4 (also known as trophoblast glycoprotein: TPBG) gene is expressed in the adult mouse tongue.Results: In immunohistochemistry of coronal tongue sections, 5T4 protein was detected at a low level exclusively in the basal part of the lingual epithelium in developing and adult mice, and at a high level particularly in foliate papillae and circumvallate papillae (CVPs). Furthermore, immunohistochemistry of the basal part of CVPs indicated that the proliferation marker PCNA (proliferating cell nuclear antigen) co-localized with 5T4. 5T4 was strongly expressed in Krt5+ epithelial progenitors and Shh+ taste precursor cells, but weakly in mature taste receptor cells. The number of proliferating cells in the CVP was higher in 5T4-knockout mice than in wild-type (WT) mice, while neither cell differentiation nor the size of taste buds differed between these two groups of mice. Notably, X-ray irradiation enhanced cell proliferation more in 5T4-knockout mice than in WT mice.Conclusion: Our results suggest that 5T4, expressed in epithelial progenitors (taste stem/progenitor cells), and taste precursor cells, may influence the maintenance of taste papillae under both normal and injury conditions.

Taste receptor cells are morphologically classified as types II and III. Type II cells form a unique type of synapses referred to as channel synapses where calcium homeostasis modulator 1 (CALHM1) together with CALHM3 forms voltage-gated channels that release the neurotransmitter, adenosine triphosphate (ATP). To validate the proposed structural model of channel synapses, the ultrastructural localization of CALHM1 in type II cells of both fungiform and circumvallate taste buds was examined. A monoclonal antibody against CALHM1 was developed and its localization was evaluated via immunofluorescence and immunoelectron microscopy using the immunogold-silver labeling technique. CALHM1 was detected as puncta using immunofluorescence and along the presynaptic membrane of channel synapses facing atypical mitochondria, which provide ATP, by immunoelectron microscopy. In addition, it was detected along the plasma membrane lined by subsurface cisternae at sites apposed to afferent nerve fibers. Our results support the validity of a previously proposed structural model for channel synapses and provide insights into the function of subsurface cisternae whose function in taste receptor cells is unknown. We also examined the localization of CALHM1 in hybrid synapses of type III cells, which are conventional chemical synapses accompanied by mitochondria similar to atypical mitochondria of channel synapses. CALHM1 was not detected in the six hybrid synapses examined using immunoelectron microscopy. We further performed double immunolabeling for CALHM1 and Bassoon, which is detected as puncta corresponding to conventional vesicular synapses in type III cells. Our observations suggest that at least some, and probably most, hybrid synapses are not accompanied by CALHM1., (© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Patients with diabetes exhibit altered taste sensitivity, but its details have not been clarified yet. Here, we examined alteration of sweet taste sensitivity with development of glucose intolerance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats as a model of non-insulin-dependent diabetes mellitus. Compared to the cases of Long Evans Tokushima Otsuka (LETO) rats as a control, glucose tolerance of OLETF rats decreased with aging, resulting in development of diabetes at 36-weeks-old. In brief-access tests with a mixture of sucrose and quinine hydrochloride, OLETF rats at 25 or more-weeks-old seemed to exhibit lower sweet taste sensitivity than age-matched LETO ones, but the lick ratios of LETO, but not OLETF, rats for the mixture and quinine hydrochloride solutions decreased and increased, respectively, aging-dependently. Expression of sweet taste receptors, T1R2 and T1R3, in circumvallate papillae (CP) was almost the same in LETO and OLETF rats at 10- and 40-weeks-old, while expression levels of a bitter taste receptor, T2R16, were greater in 40-weeks-old rats than in 10-weeks-old ones in both strains. There was no apparent morphological alteration in taste buds in CP between 10- and 40-weeks-old LETO and OLETF rats. Metagenomic analysis of gut microbiota revealed strain- and aging-dependent alteration of mucus layer-regulatory microbiota. Collectively, we concluded that the apparent higher sweet taste sensitivity in 25 or more-weeks-old OLETF rats than in age-matched LETO rats was due to the aging-dependent increase of bitter taste sensitivity in LETO rats with alteration of the gut microbiota.

Background: Multicellular taste buds located within taste papillae on the tongue mediate taste sensation. In taste papillae, taste bud cells (TBCs), such as taste receptor cells and taste precursor cells, and the surrounding lingual epithelium including epithelial progenitors (also called taste stem/progenitor cells) are maintained by continuous cell turnover throughout life. However, it remains unknown how the cells constituting taste buds proliferate and differentiate to maintain taste bud tissue. Based on in situ hybridization (ISH) screening, we demonstrated that the oncofetal antigen 5T4 (also known as trophoblast glycoprotein: TPBG) gene is expressed in the adult mouse tongue. Results: In immunohistochemistry of coronal tongue sections, 5T4 protein was detected at a low level exclusively in the basal part of the lingual epithelium in developing and adult mice, and at a high level particularly in foliate papillae and circumvallate papillae (CVPs). Furthermore, immunohistochemistry of the basal part of CVPs indicated that the proliferation marker PCNA (proliferating cell nuclear antigen) co-localized with 5T4. 5T4 was strongly expressed in Krt5+ epithelial progenitors and Shh+ taste precursor cells, but weakly in mature taste receptor cells. The number of proliferating cells in the CVP was higher in 5T4- knockout mice than in wild-type (WT) mice, while neither cell differentiation nor the size of taste buds differed between these two groups of mice. Notably, X-ray irradiation enhanced cell proliferation more in 5T4 -knockout mice than in WT mice. Conclusion: Our results suggest that 5T4, expressed in epithelial progenitors (taste stem/progenitor cells), and taste precursor cells, may influence the maintenance of taste papillae under both normal and injury conditions. [ABSTRACT FROM AUTHOR]

Mammalian taste buds emerge perinatally and most become mature 3–4 weeks after birth. Mature taste bud cells in rodents are known to be renewed by the surrounding K14+ basal epithelial cells and potentially other progenitor source(s), but the dynamics between initially developed taste buds and surrounding tissue compartments are unclear. Using the K14-Cre and Dermo1-Cre mouse lines to trace epithelial and mesenchymal cell lineages, we found that early taste buds in E18.5 and newborn mouse tongues are not derived from either lineage. At E11.5 when the tongue primordia (i.e., lingual swellings) emerge, the relatively homogeneous sonic hedgehog-expressing (Shh+) epithelial cells express Keratin (K) 8, a marker that is widely used to label taste buds. Mapping lineage of E11.0 Shh+ epithelium of the tongue rudiment with Shh-CreERT2/RFP mice demonstrated that both the early taste buds and the surrounding lingual epithelium are from the same population of progenitors – Shh+ epithelial cells of the tongue primordium. In combination with previous reports, we propose that Shh+K8+ cells in the homogeneous epithelium of tongue primordium at early embryonic stages are programmed to become taste papilla and taste bud cells. Switching off Shh and K8 expression in the Shh+ epithelial cells of the tongue primordium transforms the cells to non-gustatory cells surrounding papillae, including K14+ basal epithelial cells which will eventually contribute to the cell renewal of mature taste buds. • Early taste buds are not derived from the surrounding epithelium or mesenchyme. • Early taste buds arise from the E11.0 Shh+ epithelium of tongue primordium. • Taste buds and surrounding lingual epithelium share a common precursor population. • Taste bud initiation and taste bud maintenance utilize distinct progenitors. [ABSTRACT FROM AUTHOR]

Oral administration is widely used route of administration of drugs. The drug travels from the mouth, into the esophagus, then into the intestines. Sensing the taste is the major function of the tongue. In the formulation for pediatric & geriatric, bedridden & non-Cooperative patients, the main challenge to compounding pharmacist is to mask the taste of obnoxious and bitter drugs, result in patient non-compliance. Patients now expect and demand formulations that are pleasantly, or at least tolerable, flavored. This article reviews on taste-masking technologies and approaches for taste masking and bitterness reduction of dosage forms. [ABSTRACT FROM AUTHOR]

An ontogenetic analysis of the olfactory organ and the number and distribution of internal taste buds was carried out in two neon gobies (Elacatinus lori and Elacatinus colini) with the goal of revealing morphological trends that might inform an understanding of the roles of olfaction and taste in larval orientation behaviour. The pattern of development of the olfactory organ is unremarkable and enclosure of the olfactory epithelium occurs concurrently with metamorphosis and settlement in both species. Like other gobies, juvenile and adult E. lori and E. colini lack complex olfactory lamellae, and lack the accessory nasal sacs present in some adult gobies that could facilitate active olfactory ventilation (i.e., sniffing). A small number of internal taste buds are present at hatch with most found in the caudal region of the buccal cavity (on gill arches, roof of buccal cavity). As taste bud number increases, they demonstrate an anterior spread to the lips, buccal valves and tongue (i.e., tissue covering the basihyal). In the absence of an active ventilatory mechanism for the olfactory organs, the water that moves through the buccal cavity with cyclic gill ventilation may provide chemical cues allowing the internal taste buds to play a role in chemical‐mediated orientation and reef‐seeking behavior in pelagic larval fishes. [ABSTRACT FROM AUTHOR]

The gustatory system encodes information about chemical identity, nutritional value, and concentration of sensory stimuli before transmitting the signal from taste buds to central neurons that process and transform the signal. Deciphering the coding logic for taste quality requires examining responses at each level along the neural axis—from peripheral sensory organs to gustatory cortex. From the earliest single-fiber recordings, it was clear that some afferent neurons respond uniquely and others to stimuli of multiple qualities. There is frequently a "best stimulus" for a given neuron, leading to the suggestion that taste exhibits "labeled line coding." In the extreme, a strict "labeled line" requires neurons and pathways dedicated to single qualities (e.g. sweet, bitter, etc.). At the other end of the spectrum, "across-fiber," "combinatorial," or "ensemble" coding requires minimal specific information to be imparted by a single neuron. Instead, taste quality information is encoded by simultaneous activity in ensembles of afferent fibers. Further, "temporal coding" models have proposed that certain features of taste quality may be embedded in the cadence of impulse activity. Taste receptor proteins are often expressed in nonoverlapping sets of cells in taste buds apparently supporting "labeled lines." Yet, taste buds include both narrowly and broadly tuned cells. As gustatory signals proceed to the hindbrain and on to higher centers, coding becomes more distributed and temporal patterns of activity become important. Here, we present the conundrum of taste coding in the light of current electrophysiological and imaging techniques at several levels of the gustatory processing pathway. [ABSTRACT FROM AUTHOR]

The digestive tract histology of the false upside down catfish (Synodontis nigrita) was investigated to fill knowledge gap and provide data for further studies. The jaws were lined by stratified squamous epithelium containing eosinophilic club cells, mucous cells and lymphocytes. This epithelial covering may be related to protective function from pathogens and predators. The oesophagus presented abundant mucous cells in stratified squamous epithelium. These mucous cells help lubricate the tract during passage for food materials as the teleost lack salivary glands. The stomach was lined by simple columnar cells containing intra-epithelial lmphocytes which contribute to local immune response. The intestine was sacculated and mucosa was lined by simple columnar epithelium containing abundant goblet cells and lymphocytes. An intestine-rectal valve separated the rectum from the intestine. In conclusion, the digestive tract of the false upside down catfish (Synodontis nigrita) is adaptive to its feeding and lifestyle in the aquatic wild environment. [ABSTRACT FROM AUTHOR]

The gustation system for sweeteners is well-known to be regulated by nutritional and metabolic conditions, but there is no or little information on the underlying mechanism. Here, we examined whether elevation of the blood glucose level was involved in alteration of the expression of sweet taste receptors in circumvallate papillae (CP) and sweet taste sensitivity in male Sprague-Dawley rats. Rats under 4 h-fed conditions following 18 h-fasting exhibited elevated blood glucose levels and decreased pancreatic T1R3 expression, compared to rats after 18 h-fasting treatment, and they exhibited increased protein expression of sweet taste receptors T1R2 and T1R3 in CP. Under streptozotocin (STZ)-induced diabetes mellites (DM) conditions, the protein expression levels of T1R2 and T1R3 in CP were higher than those under control conditions, and these DM rats exhibited increased lick ratios in a low sucrose concentration range in a brief access test with a mixture of sucrose and quinine hydrochloride (QHCl). These findings indicate that the elevation of blood glucose level is a regulator for an increase in sweet taste receptor protein expression in rat CP, and such alteration in STZ-induced DM rats is involved in enhancement of their sweet taste sensitivity.