The Experts below are selected from a list of 9708 Experts worldwide ranked by ideXlab platform
Bryan D Moyer - One of the best experts on this subject based on the ideXlab platform.
-
Voltage-gated sodium channels in Taste Bud cells
BMC Neuroscience, 2009Co-Authors: Min Lu, Fernando Echeverri, Bianca Laita, Dalia Kalabat, Mark E Williams, Peter Hevezi, Albert Zlotnik, Bryan D MoyerAbstract:Background Taste Bud cells transmit information regarding the contents of food from Taste receptors embedded in apical microvilli to gustatory nerve fibers innervating basolateral membranes. In particular, Taste cells depolarize, activate voltage-gated sodium channels, and fire action potentials in response to tastants. Initial cell depolarization is attributable to sodium influx through TRPM5 in sweet, bitter, and umami cells and an undetermined cation influx through an ion channel in sour cells expressing PKD2L1, a candidate sour Taste receptor. The molecular identity of the voltage-gated sodium channels that sense depolarizing signals and subsequently initiate action potentials coding Taste information to gustatory nerve fibers is unknown. Results We describe the molecular and histological expression profiles of cation channels involved in electrical signal transmission from apical to basolateral membrane domains. TRPM5 was positioned immediately beneath tight junctions to receive calcium signals originating from sweet, bitter, and umami receptor activation, while PKD2L1 was positioned at the Taste pore. Using mouse Taste Bud and lingual epithelial cells collected by laser capture microdissection, SCN2A, SCN3A, and SCN9A voltage-gated sodium channel transcripts were expressed in Taste tissue. SCN2A, SCN3A, and SCN9A were expressed beneath tight junctions in subsets of Taste cells. SCN3A and SCN9A were expressed in TRPM5 cells, while SCN2A was expressed in TRPM5 and PKD2L1 cells. HCN4, a gene previously implicated in sour Taste, was expressed in PKD2L1 cells and localized to cell processes beneath the Taste pore. Conclusion SCN2A, SCN3A and SCN9A voltage-gated sodium channels are positioned to sense initial depolarizing signals stemming from Taste receptor activation and initiate Taste cell action potentials. SCN2A, SCN3A and SCN9A gene products likely account for the tetrodotoxin-sensitive sodium currents in Taste receptor cells.
-
voltage gated sodium channels in Taste Bud cells
BMC Neuroscience, 2009Co-Authors: Na Gao, Fernando Echeverri, Bianca Laita, Dalia Kalabat, Peter Hevezi, Albert Zlotnik, Mark Williams, Bryan D MoyerAbstract:Background Taste Bud cells transmit information regarding the contents of food from Taste receptors embedded in apical microvilli to gustatory nerve fibers innervating basolateral membranes. In particular, Taste cells depolarize, activate voltage-gated sodium channels, and fire action potentials in response to tastants. Initial cell depolarization is attributable to sodium influx through TRPM5 in sweet, bitter, and umami cells and an undetermined cation influx through an ion channel in sour cells expressing PKD2L1, a candidate sour Taste receptor. The molecular identity of the voltage-gated sodium channels that sense depolarizing signals and subsequently initiate action potentials coding Taste information to gustatory nerve fibers is unknown.
David L Hill - One of the best experts on this subject based on the ideXlab platform.
-
fungiform Taste Bud degeneration in c57bl 6j mice following chorda lingual nerve transection
The Journal of Comparative Neurology, 2007Co-Authors: Nick A Guagliardo, David L HillAbstract:Taste Buds are dependent on innervation for normal morphology and function. Fungiform Taste Bud degeneration after chorda tympani nerve injury has been well documented in rats, hamsters, and gerbils. The current study examines fungiform Taste Bud distribution and structure in adult C57BL/6J mice from both intact Taste systems and after unilateral chorda-lingual nerve transection. Fungiform Taste Buds were visualized and measured with the aid of cytokeratin 8. In control mice, Taste Buds were smaller and more abundant on the anterior tip (<1 mm) of the tongue. By 5 days after nerve transection Taste Buds were smaller and fewer on the side of the tongue ipsilateral to the transection and continued to decrease in both size and number until 15 days posttransection. Degenerating fungiform Taste Buds were smaller due to a loss of Taste Bud cells rather than changes in Taste Bud morphology. While almost all Taste Buds disappeared in more posterior fungiform papillae by 15 days posttransection, the anterior tip of the tongue retained nearly half of its Taste Buds compared to intact mice. Surviving Taste Buds could not be explained by an apparent innervation from the remaining intact nerves. Contralateral effects of nerve transection were also observed; Taste Buds were larger due to an increase in the number of Taste Bud cells. These data are the first to characterize adult mouse fungiform Taste Buds and subsequent degeneration after unilateral nerve transection. They provide the basis for more mechanistic studies in which genetically engineered mice can be used.
-
Fungiform Taste Bud degeneration in C57BL/6J mice following chorda-lingual nerve transection.
The Journal of comparative neurology, 2007Co-Authors: Nick A Guagliardo, David L HillAbstract:Taste Buds are dependent on innervation for normal morphology and function. Fungiform Taste Bud degeneration after chorda tympani nerve injury has been well documented in rats, hamsters, and gerbils. The current study examines fungiform Taste Bud distribution and structure in adult C57BL/6J mice from both intact Taste systems and after unilateral chorda-lingual nerve transection. Fungiform Taste Buds were visualized and measured with the aid of cytokeratin 8. In control mice, Taste Buds were smaller and more abundant on the anterior tip (
-
Taste Bud cell dynamics during normal and sodium-restricted development.
The Journal of comparative neurology, 2004Co-Authors: Susan J. Hendricks, Peter C. Brunjes, David L HillAbstract:Taste Bud volume increases over the postnatal period to match the number of neurons providing innervation. To clarify age-related changes in fungiform Taste Bud volume, the current study investigated developmental changes in Taste Bud cell number, proliferation rate, and life span. Taste Bud growth can largely be accounted for by addition of cytokeratin-19-positive Taste Bud cells. Examination of Taste Bud cell kinetics with 3H-thymidine autoradiography revealed that cell life span and turnover periods were not altered during normal development but that cells were produced more rapidly in young rats, a prominent modification that could lead to increased Taste Bud size. By comparison, dietary sodium restriction instituted during pre- and postnatal development results in small Taste Buds at adulthood as a result of fewer cytokeratin-19-positive cells. The dietary manipulation also had profound influences on Taste Bud growth kinetics, including an increased latency for cells to enter the Taste Bud and longer life span and turnover periods. These studies provide fundamental, new information about Taste Bud development under normal conditions and after environmental manipulations that impact nerve/target matching. J. Comp. Neurol. 472:173–182, 2004. © 2004 Wiley-Liss, Inc.
-
Quantitative Relationships between Taste Bud Development and Gustatory Ganglion Cellsa
Annals of the New York Academy of Sciences, 1998Co-Authors: Robin F. Krimm, David L HillAbstract:: To determine whether patterns of Taste Bud innervation change during postnatal rat development, the number of geniculate ganglion cells that innervate single Taste Buds were quantified in adult and developing rats. While there was a large variation in numbers of ganglion cells that innervate individual Taste Buds, there was a high degree of organization in the system. Namely, the number of labeled geniculate ganglion cells innervating a Taste Bud was highly correlated with the size of the Taste Bud. This relationship between Taste Bud size and number of innervating ganglion cells develops over a prolonged postnatal period and is not established until postnatal day 40 (P40), when Taste Buds reach their adult size. In a second series of experiments, we sought to determine whether neural rearrangement of chorda tympani neurons is responsible for the development of this relationship by double-labeling single Taste Buds at different ages. We found that the number of ganglion cells innervating individual Taste Buds on P10 predicts the size that Taste Buds become by P40. This finding suggests that neural rearrangement is not responsible for establishing the relationship between Taste Bud size and the number of innervating ganglion cells during development. More importantly, it strongly suggests that the 'neural template' for the mature innervation pattern is determined during early postnatal development.
Yoshitaka Ohtubo - One of the best experts on this subject based on the ideXlab platform.
-
Quantitative Analysis of Taste Bud Cell Numbers in the Circumvallate and Foliate Taste Buds of Mice.
Chemical senses, 2020Co-Authors: Takahiro Ogata, Yoshitaka OhtuboAbstract:A mouse single Taste Bud contains 10-100 Taste Bud cells (TBCs) in which the elongated TBCs are classified into 3 cell types (types I-III) equipped with different Taste receptors. Accordingly, differences in the cell numbers and ratios of respective cell types per Taste Bud may affect Taste-nerve responsiveness. Here, we examined the numbers of each immunoreactive cell for the type II (sweet, bitter, or umami receptor cells) and type III (sour and/or salt receptor cells) markers per Taste Bud in the circumvallate and foliate papillae and compared these numerical features of TBCs per Taste Bud to those in fungiform papilla and soft palate, which we previously reported. In circumvallate and foliate Taste Buds, the numbers of TBCs and immunoreactive cells per Taste Bud increased as a linear function of the maximal cross-sectional Taste Bud area. Type II cells made up approximately 25% of TBCs irrespective of the regions from which the TBCs arose. In contrast, type III cells in circumvallate and foliate Taste Buds made up approximately 11% of TBCs, which represented almost 2 times higher than what was observed in the fungiform and soft palate Taste Buds. The densities (number of immunoreactive cells per Taste Bud divided by the maximal cross-sectional area of the Taste Bud) of types II and III cells per Taste Bud are significantly higher in the circumvallate papillae than in the other regions. The effects of these region-dependent differences on the Taste response of the Taste Bud are discussed.
-
Selective expression of muscarinic acetylcholine receptor subtype M3 by mouse type III Taste Bud cells
Pflügers Archiv - European Journal of Physiology, 2016Co-Authors: Yusuke Mori, Kazuki Yoshii, Kinya Eguchi, Yoshitaka OhtuboAbstract:Each Taste Bud cell (TBC) type responds to a different Taste. Previously, we showed that an unidentified cell type(s) functionally expresses a muscarinic acetylcholine (ACh) receptor subtype, M3, and we suggested the ACh-dependent modification of its Taste responsiveness. In this study, we found that M3 is expressed by type III TBCs, which is the only cell type that possesses synaptic contacts with Taste nerve fibers in Taste Buds. The application of ACh to the basolateral membrane of mouse fungiform TBCs in situ increased the intracellular Ca2+ concentration in 2.4 ± 1.4 cells per Taste Bud (mean ± SD, n = 14). After Ca2+ imaging, we supravitally labeled type II cells (phospholipase C β2 [PLCβ2]-immunoreactive cells) with Lucifer yellow CH (LY), a fluorescent dye and investigated the positional relationship between ACh-responding cells and LY-labeled cells. After fixation, the TBCs were immunohistostained to investigate the positional relationships between immunohistochemically classified cells and LY-labeled cells. The overlay of the two positional relationships obtained by superimposing the LY-labeled cells showed that all of the ACh-responding cells were type III cells (synaptosomal-associated protein 25 [SNAP-25]-immunoreactive cells). The ACh responses required no added Ca2+ in the bathing solution. The addition of 1 μM U73122, a phospholipase C inhibitor, decreased the magnitude of the ACh response, whereas that of 1 μM U73343, a negative control, had no effect. These results suggest that type III cells respond to ACh and release Ca2+ from intracellular stores. We also discuss the underlying mechanism of the Ca2+ response and the role of M3 in type III cells.
-
Quantitative analysis of Taste Bud cell numbers in fungiform and soft palate Taste Buds of mice
Brain research, 2010Co-Authors: Yoshitaka Ohtubo, Kiyonori YoshiiAbstract:Mammalian Taste Bud cells (TBCs) consist of several cell types equipped with different Taste receptor molecules, and hence the ratio of cell types in a Taste Bud constitutes the Taste responses of the Taste Bud. Here we show that the population of immunohistochemically identified cell types per Taste Bud is proportional to the number of total TBCs in the Taste Bud or the area of the Taste Bud in fungiform papillae, and that the proportions differ among cell types. This result is applicable to soft palate Taste Buds. However, the density of almost all cell types, the population of cell types divided by the area of the respective Taste Buds, is significantly higher in soft palates. These results suggest that the turnover of TBCs is regulated to keep the ratio of each cell type constant, and that Taste responsiveness is different between fungiform and soft palate Taste Buds.
-
functional expression of ionotropic purinergic receptors on mouse Taste Bud cells
The Journal of Physiology, 2007Co-Authors: Ryotaro Hayato, Yoshitaka Ohtubo, Kiyonori YoshiiAbstract:Neurotransmitter receptors on Taste Bud cells (TBCs) and Taste nerve fibres are likely to contribute to Taste transduction by mediating the interaction among TBCs and that between TBCs and Taste nerve fibres. We investigated the functional expression of P2 receptor subtypes on TBCs of mouse fungiform papillae. Electrophysiological studies showed that 100 μm ATP applied to their basolateral membranes either depolarized or hyperpolarized a few cells per Taste Bud. Ca2+ imaging showed that similarly applied 1 μm ATP, 30 μm BzATP (a P2X7 agonist), or 1 μm 2MeSATP (a P2Y1 and P2Y11 agonist) increased intracellular Ca2+ concentration, but 100 μm UTP (a P2Y2 and P2Y4 agonist) and α,β-meATP (a P2X agonist except for P2X2, P2X4 and P2X7) did not. RT-PCR suggested the expression of P2X2, P2X4, P2X7, P2Y1, P2Y13 and P2Y14 among the seven P2X subtypes and seven P2Y subtypes examined. Immunohistostaining confirmed the expression of P2X2. The exposure of the basolateral membranes to 3 mm ATP for 30 min caused the uptake of Lucifer Yellow CH in a few TBCs per Taste Bud. This was antagonized by 100 μm PPADS (a non-selective P2 blocker) and 1 μm KN-62 (a P2X7 blocker). These results showed for the first time the functional expression of P2X2 and P2X7 on TBCs. The roles of P2 receptor subtypes in the Taste transduction, and the renewal of TBCs, are discussed.
-
a network model toward a Taste Bud inspired sensor
International Congress Series, 2007Co-Authors: Katsumi Tateno, Yoshitaka Ohtubo, Kiyonori Yoshii, Tsutomu MikiAbstract:Abstract This study shows a computational model of a Taste-sensing system inspired by physiological properties of mammalian Taste organs. The experimental results indicated that the Taste Bud cells (TBCs) form cell networks within single Taste Buds. The computational model includes those cell networks between Taste-sensing cells (leaky integrate-and-fire (LIAF) model) and output cells (bursting cell model). Each LIAF model was heterogeneous. Outputs of a plurality of the LIAF models were integrated in the bursting cells. The dc bias current caused irregular interbeat intervals in the LIAF models. Noisy input from the LIAF models induced synchronization in the bursting cells. The degree of synchronization between the bursting cells was considered output of the network. The degree of synchronization increased with an increase in the mean dc current in the LIAF models. Although we do not know how the Taste stimuli charge the LIAF models, the present network model potentially detects the Taste stimuli as the degree of synchronization of TBCs.
Linda A. Barlow - One of the best experts on this subject based on the ideXlab platform.
-
sonic hedgehog from both nerves and epithelium is a key trophic factor for Taste Bud maintenance
Development, 2017Co-Authors: David Castilloazofeifa, Justin T Losacco, Ernesto Salcedo, Erin Golden, Thomas E Finger, Linda A. BarlowAbstract:The integrity of Taste Buds is intimately dependent on an intact gustatory innervation, yet the molecular nature of this dependency is unknown. Here, we show that differentiation of new Taste Bud cells, but not progenitor proliferation, is interrupted in mice treated with a hedgehog (Hh) pathway inhibitor (HPI), and that gustatory nerves are a source of sonic hedgehog (Shh) for Taste Bud renewal. Additionally, epithelial Taste precursor cells express Shh transiently, and provide a local supply of Hh ligand that supports Taste cell renewal. Taste Buds are minimally affected when Shh is lost from either tissue source. However, when both the epithelial and neural supply of Shh are removed, Taste Buds largely disappear. We conclude Shh supplied by Taste nerves and local Taste epithelium act in concert to support continued Taste Bud differentiation. However, although neurally derived Shh is in part responsible for the dependence of Taste cell renewal on gustatory innervation, neurotrophic support of Taste Buds likely involves a complex set of factors.
-
β-catenin is required for Taste Bud cell renewal and behavioral Taste perception in adult mice.
PLOS Genetics, 2017Co-Authors: Dany Gaillard, Spencer G. Bowles, Ernesto E. Salcedo, Sarah E Millar, Mingang Xu, Linda A. BarlowAbstract:Taste stimuli are transduced by Taste Buds and transmitted to the brain via afferent gustatory fibers. Renewal of Taste receptor cells from actively dividing progenitors is finely tuned to maintain Taste sensitivity throughout life. We show that conditional β-catenin deletion in mouse Taste progenitors leads to rapid depletion of progenitors and Shh+ precursors, which in turn causes Taste Bud loss, followed by loss of gustatory nerve fibers. In addition, our data suggest LEF1, TCF7 and Wnt3 are involved in a Wnt pathway regulatory feedback loop that controls Taste cell renewal in the circumvallate papilla epithelium. Unexpectedly, Taste Bud decline is greater in the anterior tongue and palate than in the posterior tongue. Mutant mice with this regional pattern of Taste Bud loss were unable to discern sweet at any concentration, but could distinguish bitter stimuli, albeit with reduced sensitivity. Our findings are consistent with published reports wherein anterior Taste Buds have higher sweet sensitivity while posterior Taste Buds are better tuned to bitter, and suggest β-catenin plays a greater role in renewal of anterior versus posterior Taste Buds.
-
β catenin signaling regulates temporally discrete phases of anterior Taste Bud development
Development, 2015Co-Authors: Shoba Thirumangalathu, Linda A. BarlowAbstract:The sense of Taste is mediated by multicellular Taste Buds located within Taste papillae on the tongue. In mice, individual Taste Buds reside in fungiform papillae, which develop at mid-gestation as epithelial placodes in the anterior tongue. Taste placodes comprise Taste Bud precursor cells, which express the secreted factor sonic hedgehog (Shh) and give rise to Taste Bud cells that differentiate around birth. We showed previously that epithelial activation of β-catenin is the primary inductive signal for Taste placode formation, followed by Taste papilla morphogenesis and Taste Bud differentiation, but the degree to which these later elements were direct or indirect consequences of β-catenin signaling was not explored. Here, we define discrete spatiotemporal functions of β-catenin in fungiform Taste Bud development. Specifically, we show that early epithelial activation of β-catenin, before Taste placodes form, diverts lingual epithelial cells from a Taste Bud fate. By contrast, β-catenin activation a day later within Shh(+) placodes, expands Taste Bud precursors directly, but enlarges papillae indirectly. Further, placodal activation of β-catenin drives precocious differentiation of Type I glial-like Taste cells, but not other Taste cell types. Later activation of β-catenin within Shh(+) precursors during papilla morphogenesis also expands Taste Bud precursors and accelerates Type I cell differentiation, but papilla size is no longer enhanced. Finally, although Shh regulates Taste placode patterning, we find that it is dispensable for the accelerated Type I cell differentiation induced by β-catenin.
-
Fate mapping of mammalian embryonic Taste Bud progenitors
Development (Cambridge England), 2009Co-Authors: Shoba Thirumangalathu, Robin F. Krimm, Danielle E. Harlow, Amanda L. Driskell, Linda A. BarlowAbstract:Mammalian Taste Buds have properties of both epithelial and neuronal cells, and are thus developmentally intriguing. Taste Buds differentiate at birth within epithelial appendages, termed Taste papillae, which arise at mid-gestation as epithelial thickenings or placodes. However, the embryonic relationship between placodes, papillae and adult Taste Buds has not been defined. Here, using an inducible Cre-lox fate mapping approach with the ShhcreERT2 mouse line, we demonstrate that Shh-expressing embryonic Taste placodes are Taste Bud progenitors, which give rise to at least two different adult Taste cell types, but do not contribute to Taste papillae. Strikingly, placodally descendant Taste cells disappear early in adult life. As placodally derived Taste cells are lost, we used Wnt1Cre mice to show that the neural crest does not supply cells to Taste Buds, either embryonically or postnatally, thus ruling out a mesenchymal contribution to Taste Buds. Finally, using Bdnf null mice, which lose neurons that innervate Taste Buds, we demonstrate that Shh-expressing Taste Bud progenitors are specified and produce differentiated Taste cells normally, in the absence of gustatory nerve contact. This resolution of a direct relationship between embryonic Taste placodes with adult Taste Buds, which is independent of mesenchymal contribution and nerve contact, allows us to better define the early development of this important sensory system. These studies further suggest that mammalian Taste Bud development is very distinct from that of other epithelial appendages.
-
Amphibians provide new insights into Taste-Bud development
Trends in neurosciences, 1998Co-Authors: R. Glenn Northcutt, Linda A. BarlowAbstract:Until recently, the predominant model of Taste-Bud development was one of neural induction: ingrowing sensory fibers were thought to induce Taste-Bud differentiation late in embryonic development. Recent experimental studies, however, show that the development of Taste Buds is independent of their innervation. In amphibian embryos, the ability to generate Taste Buds is an intrinsic feature of the oropharyngeal epithelium long before the region becomes innervated. These studies indicate that patterning of the oropharyngeal epithelium occurs during gastrulation, and suggest that Taste Buds or their progenitors play the dominant role in the development of their own innervation.
Bronwen Martin - One of the best experts on this subject based on the ideXlab platform.
-
longitudinal analysis of calorie restriction on rat Taste Bud morphology and expression of sweet Taste modulators
Journals of Gerontology Series A-biological Sciences and Medical Sciences, 2014Co-Authors: Huan Cai, Weina Cong, Stuart Maudsley, Caitlin M Daimon, Rui Wang, Patrick Chirdon, Rafael De Cabo, Jean Sevigny, Bronwen MartinAbstract:Calorie restriction (CR) is a lifestyle intervention employed to reduce body weight and improve metabolic functions primarily via reduction of ingested carbohydrates and fats. Taste perception is highly related to functional metabolic status and body adiposity. We have previously shown that sweet Taste perception diminishes with age; however, relatively little is known about the effects of various lengths of CR upon Taste cell morphology and function. We investigated the effects of CR on Taste Bud morphology and expression of sweet Taste–related modulators in 5-, 17-, and 30-month-old rats. In ad libitum (AL) and CR rats, we consistently found the following parameters altered significantly with advancing age: reduction of Taste Bud size and Taste cell numbers per Taste Bud and reduced expression of sonic hedgehog, type 1 Taste receptor 3 (T1r3), α-gustducin, and glucagon-like peptide-1 (GLP-1). In the oldest rats, CR affected a significant reduction of tongue T1r3, GLP-1, and α-gustducin expression compared with age-matched AL rats. Leptin receptor immunopositive cells were elevated in 17- and 30-month-old CR rats compared with age-matched AL rats. These alterations of sweet Taste–related modulators, specifically during advanced aging, suggest that sweet Taste perception may be altered in response to different lengths of CR.
-
age related changes in mouse Taste Bud morphology hormone expression and Taste responsivity
Journals of Gerontology Series A-biological Sciences and Medical Sciences, 2012Co-Authors: Yu Kyong Shin, Josephine M Egan, Weina Cong, Huan Cai, Wook Kim, Stuart Maudsley, Bronwen MartinAbstract:Normal aging is a complex process that affects every organ system in the body, including the Taste system. Thus, we investigated the effects of the normal aging process on Taste Bud morphology, function, and Taste responsivity in male mice at 2, 10, and 18 months of age. The 18-month-old animals demonstrated a significant reduction in Taste Bud size and number of Taste cells per Bud compared with the 2- and 10-month-old animals. The 18-month-old animals exhibited a significant reduction of protein gene product 9.5 and sonic hedgehog immunoreactivity (Taste cell markers). The number of Taste cells expressing the sweet Taste receptor subunit, T1R3, and the sweet Taste modulating hormone, glucagon-like peptide-1, were reduced in the 18-month-old mice. Concordant with Taste cell alterations, the 18-month-old animals demonstrated reduced sweet Taste responsivity compared with the younger animals and the other major Taste modalities (salty, sour, and bitter) remained intact.
