Talk:Sensory - Taste Development
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Cite this page: Hill, M.A. (2024, April 19) Embryology Sensory - Taste Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Sensory_-_Taste_Development |
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Taste Bud Development
<pubmed limit=5>Taste Bud Development</pubmed>
Tongue Development
<pubmed limit=5>Tongue Development</pubmed>
2014
BDNF and NT4 play interchangeable roles in gustatory development
Dev Biol. 2014 Feb 15;386(2):308-20. doi: 10.1016/j.ydbio.2013.12.031. Epub 2013 Dec 27.
Huang T1, Krimm RF2. Author information
Abstract A limited number of growth factors are capable of regulating numerous developmental processes, but how they accomplish this is unclear. The gustatory system is ideal for examining this issue because the neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT4) have different developmental roles although both of them activate the same receptors, TrkB and p75. Here we first investigated whether the different roles of BDNF and NT4 are due to their differences in temporal and spatial expression patterns. Then, we asked whether or not these two neurotrophins exert their unique roles on the gustatory system by regulating different sets of downstream genes. By using Bdnf(Nt4/Nt4) mice, in which the coding region for BDNF is replaced with NT4, we examined whether the different functions of BDNF and NT4 are interchangeable during taste development. Our results demonstrated that NT4 could mediate most of the unique roles of BDNF during taste development. Specifically, caspase-3-mediated cell death, which was increased in the geniculate ganglion in Bdnf(-/-) mice, was rescued in Bdnf(Nt4/Nt4) mice. In BDNF knockout mice, tongue innervation was disrupted, and gustatory axons failed to reach their targets. However, disrupted innervation was rescued and target innervation is normal when NT4 replaced BDNF. Genome wide expression analyses revealed that BDNF and NT4 mutant mice exhibited different gene expression profiles in the gustatory (geniculate) ganglion. Compared to wild type, the expression of differentiation-, apoptosis- and axon guidance-related genes was changed in BDNF mutant mice, which is consistent with their different roles during taste development. However, replacement of BDNF by NT4 rescued these gene expression changes. These findings indicate that the functions of BDNF and NT4 in taste development are interchangeable. Spatial and temporal differences in BDNF and NT4 expression can regulate differential gene expression in vivo and determine their specific roles during development. Copyright © 2014 Elsevier Inc. All rights reserved. KEYWORDS: Brain derived neurotrophic factor, Geniculate ganglion neurons, Neurotrophin-4, Neurotrophins, Taste
PMID 24378336
2013
Taste Neurons Consist of Both a Large TrkB-Receptor-Dependent and a Small TrkB-Receptor-Independent Subpopulation
PLoS One. 2013 Dec 27;8(12):e83460. doi: 10.1371/journal.pone.0083460. eCollection 2013.
Fei D, Krimm RF. Author information
Abstract
Brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4) are two neurotrophins that play distinct roles in geniculate (taste) neuron survival, target innervation, and taste bud formation. These two neurotrophins both activate the tropomyosin-related kinase B (TrkB) receptor and the pan-neurotrophin receptor p75. Although the roles of these neurotrophins have been well studied, the degree to which BDNF and NT-4 act via TrkB to regulate taste development in vivo remains unclear. In this study, we compared taste development in TrkB(-/-) and Bdnf(-/-)/Ntf4(-/-) mice to determine if these deficits were similar. If so, this would indicate that the functions of both BDNF and NT-4 can be accounted for by TrkB-signaling. We found that TrkB(-/-) and Bdnf(-/-)/Ntf4(-/-) mice lose a similar number of geniculate neurons by E13.5, which indicates that both BDNF and NT-4 act primarily via TrkB to regulate geniculate neuron survival. Surprisingly, the few geniculate neurons that remain in TrkB(-/-) mice are more successful at innervating the tongue and taste buds compared with those neurons that remain in Bdnf(-/-)/Ntf4(-/-) mice. The remaining neurons in TrkB(-/-) mice support a significant number of taste buds. In addition, these remaining neurons do not express the TrkB receptor, which indicates that either BDNF or NT-4 must act via additional receptors to influence tongue innervation and/or targeting. PMID 24386206
CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes
Nature. 2013 Mar 6. doi: 10.1038/nature11906.
Taruno A, Vingtdeux V, Ohmoto M, Ma Z, Dvoryanchikov G, Li A, Adrien L, Zhao H, Leung S, Abernethy M, Koppel J, Davies P, Civan MM, Chaudhari N, Matsumoto I, Hellekant G, Tordoff MG, Marambaud P, Foskett JK. Source 1] Department of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA [2].
Abstract
Recognition of sweet, bitter and umami tastes requires the non-vesicular release from taste bud cells of ATP, which acts as a neurotransmitter to activate afferent neural gustatory pathways. However, how ATP is released to fulfil this function is not fully understood. Here we show that calcium homeostasis modulator 1 (CALHM1), a voltage-gated ion channel, is indispensable for taste-stimuli-evoked ATP release from sweet-, bitter- and umami-sensing taste bud cells. Calhm1 knockout mice have severely impaired perceptions of sweet, bitter and umami compounds, whereas their recognition of sour and salty tastes remains mostly normal. Calhm1 deficiency affects taste perception without interfering with taste cell development or integrity. CALHM1 is expressed specifically in sweet/bitter/umami-sensing type II taste bud cells. Its heterologous expression induces a novel ATP permeability that releases ATP from cells in response to manipulations that activate the CALHM1 ion channel. Knockout of Calhm1 strongly reduces voltage-gated currents in type II cells and taste-evoked ATP release from taste buds without affecting the excitability of taste cells by taste stimuli. Thus, CALHM1 is a voltage-gated ATP-release channel required for sweet, bitter and umami taste perception.
PMID 23467090
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11906.html
2012
Developing a sense of taste
Semin Cell Dev Biol. 2012 Nov 24. pii: S1084-9521(12)00204-2. doi: 10.1016/j.semcdb.2012.11.002. [Epub ahead of print]
Kapsimali M, Barlow LA. Source Ecole Normale Superieure, Institut de Biologie, 75005 Paris, France; INSERM U1024, 75005 Paris, France; CNRS UMR8197, 75005 Paris, France. Electronic address: marika.kapsimali@ens.fr. Abstract Taste buds are found in a distributed array on the tongue surface, and are innervated by cranial nerves that convey taste information to the brain. For nearly a century, taste buds were thought to be induced by nerves late in embryonic development. However, this view has shifted dramatically. A host of studies now indicate that taste bud development is initiated and proceeds via processes that are nerve-independent, occur long before birth, and governed by cellular and molecular mechanisms intrinsic to the developing tongue. Here we review the state of our understanding of the molecular and cellular regulation of taste bud development, incorporating important new data obtained through the use of two powerful genetic systems, mouse and zebrafish. Copyright © 2012 Elsevier Ltd. All rights reserved.
PMID 23182899
Neural crest contribution to lingual mesenchyme, epithelium and developing taste papillae and taste buds
Dev Biol. 2012 Aug 15;368(2):294-303. doi: 10.1016/j.ydbio.2012.05.028. Epub 2012 May 31.
Liu HX, Komatsu Y, Mishina Y, Mistretta CM. Source Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI, USA. lhx@umich.edu
Abstract
The epithelium of mammalian tongue hosts most of the taste buds that transduce gustatory stimuli into neural signals. In the field of taste biology, taste bud cells have been described as arising from "local epithelium", in distinction from many other receptor organs that are derived from neurogenic ectoderm including neural crest (NC). In fact, contribution of NC to both epithelium and mesenchyme in the developing tongue is not fully understood. In the present study we used two independent, well-characterized mouse lines, Wnt1-Cre and P0-Cre that express Cre recombinase in a NC-specific manner, in combination with two Cre reporter mouse lines, R26R and ZEG, and demonstrate a contribution of NC-derived cells to both tongue mesenchyme and epithelium including taste papillae and taste buds. In tongue mesenchyme, distribution of NC-derived cells is in close association with taste papillae. In tongue epithelium, labeled cells are observed in an initial scattered distribution and progress to a clustered pattern between papillae, and within papillae and early taste buds. This provides evidence for a contribution of NC to lingual epithelium. Together with previous reports for the origin of taste bud cells from local epithelium in postnatal mouse, we propose that NC cells migrate into and reside in the epithelium of the tongue primordium at an early embryonic stage, acquire epithelial cell phenotypes, and undergo cell proliferation and differentiation that is involved in the development of taste papillae and taste buds. Our findings lead to a new concept about derivation of taste bud cells that include a NC origin. Copyright © 2012 Elsevier Inc. All rights reserved.
PMID 22659543
2011
FGF Signaling Regulates the Number of Posterior Taste Papillae by Controlling Progenitor Field Size
PLoS Genet. 2011 Jun;7(6):e1002098. Epub 2011 Jun 2.
Petersen CI, Jheon AH, Mostowfi P, Charles C, Ching S, Thirumangalathu S, Barlow LA, Klein OD. Source
Department of Orofacial Sciences and Program in Craniofacial and Mesenchymal Biology, University of California San Francisco, San Francisco, California, United States of America. Abstract
The sense of taste is fundamental to our ability to ingest nutritious substances and to detect and avoid potentially toxic ones. Sensory taste buds are housed in papillae that develop from epithelial placodes. Three distinct types of gustatory papillae reside on the rodent tongue: small fungiform papillae are found in the anterior tongue, whereas the posterior tongue contains the larger foliate papillae and a single midline circumvallate papilla (CVP). Despite the great variation in the number of CVPs in mammals, its importance in taste function, and its status as the largest of the taste papillae, very little is known about the development of this structure. Here, we report that a balance between Sprouty (Spry) genes and Fgf10, which respectively antagonize and activate receptor tyrosine kinase (RTK) signaling, regulates the number of CVPs. Deletion of Spry2 alone resulted in duplication of the CVP as a result of an increase in the size of the placode progenitor field, and Spry1(-/-);Spry2(-/-) embryos had multiple CVPs, demonstrating the redundancy of Sprouty genes in regulating the progenitor field size. By contrast, deletion of Fgf10 led to absence of the CVP, identifying FGF10 as the first inductive, mesenchyme-derived factor for taste papillae. Our results provide the first demonstration of the role of epithelial-mesenchymal FGF signaling in taste papilla development, indicate that regulation of the progenitor field size by FGF signaling is a critical determinant of papilla number, and suggest that the great variation in CVP number among mammalian species may be linked to levels of signaling by the FGF pathway.
PMID 21655085
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3107195 http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002098
The study of postnatal and later development of the taste and olfactory systems using the human brain mapping approach: an update
Brain Res Bull. 2011 Feb 1;84(2):118-24. Epub 2010 Dec 22.
Domínguez PR.
University of Granada, Experimental Psychology and Physiology of Behavior, Granada, Spain. palomaroh@ugr.es
Abstract Gustatory and olfactory functions are already present at birth, although the full development of both systems takes place postnatally. The existence of early postnatal sensitive periods throughout the developmental course of sensory systems, including the taste and olfactory, has been well documented. The normal postnatal and later development of any sensory function parallels development of the central nervous system. This development is associated with development-related plastic changes that ensure the increasing efficiency of neural communication that takes place throughout development and correlates with signal changes acquired by means of neuroimaging techniques. In this paper, we review papers published in the last 10 years that have reported on the investigation of age-related changes in brain activation patterns in response to gustatory and olfactory processing with two related aims. We aim to ascertain the way in which developmental plastic changes within the taste and olfactory systems have been reflected in signals obtained through neuroimaging techniques. Furthermore, we aim to identify sensitive periods of gustatory and olfactory development by conducting a systematic review of research on brain activation patterns of the taste and olfactory systems that have been measured through neuroimaging techniques in developing populations. The main contribution of the present review is the identification of the need to conduct further research on developmental brain mapping of the taste and olfactory systems in newborns, children and adolescents, and on the association between developmental plastic changes and imaging signals. In addition, further developmental research based on longitudinal designs is required.
Copyright © 2010 Elsevier Inc. All rights reserved.
PMID 21184814
2010
Differential expression of a BMP4 reporter allele in anterior fungiform versus posterior circumvallate taste buds of mice
BMC Neurosci. 2010 Oct 13;11:129.
Nguyen HM, Barlow LA.
Rocky Mountain Taste and Smell Center, Department of Cell and Developmental Biology, University of Colorado Denver, School of Medicine, Aurora, Colorado 80045, USA. Abstract BACKGROUND: Bone Morphogenetic Protein 4 (BMP4) is a diffusible factor which regulates embryonic taste organ development. However, the role of BMP4 in taste buds of adult mice is unknown. We utilized transgenic mice with LacZ under the control of the BMP4 promoter to reveal the expression of BMP4 in the tongues of adult mice. Further we evaluate the pattern of BMP4 expression with that of markers of specific taste bud cell types and cell proliferation to define and compare the cell populations expressing BMP4 in anterior (fungiform papillae) and posterior (circumvallate papilla) tongue.
RESULTS: BMP4 is expressed in adult fungiform and circumvallate papillae, i.e., lingual structures composed of non-taste epithelium and taste buds. Unexpectedly, we find both differences and similarities with respect to expression of BMP4-driven ß-galactosidase. In circumvallate papillae, many fusiform cells within taste buds are BMP4-ß-gal positive. Further, a low percentage of BMP4-expressing cells within circumvallate taste buds is immunopositive for markers of each of the three differentiated taste cell types (I, II and III). BMP4-positive intragemmal cells also expressed a putative marker of immature taste cells, Sox2, and consistent with this finding, intragemmal cells expressed BMP4-ß-gal within 24 hours after their final mitosis, as determined by BrdU birthdating. By contrast, in fungiform papillae, BMP4-ß-gal positive cells are never encountered within taste buds. However, in both circumvallate and fungiform papillae, BMP4-ß-gal expressing cells are located in the perigemmal region, comprising basal and edge epithelial cells adjacent to taste buds proper. This region houses the proliferative cell population that gives rise to adult taste cells. However, perigemmal BMP4-ß-gal cells appear mitotically silent in both fungiform and circumvallate taste papillae, as we do not find evidence of their active proliferation using cell cycle immunomarkers and BrdU birthdating.
CONCLUSION: Our data suggest that intragemmal BMP4-ß-gal cells in circumvallate papillae are immature taste cells which eventually differentiate into each of the 3 taste cell types, whereas perigemmal BMP4-ß-gal cells in both circumvallate and fungiform papillae may be slow cycling stem cells, or belong to the stem cell niche to regulate taste cell renewal from the proliferative cell population.
PMID 20942907
Oxytocin Signaling in Mouse Taste Buds
PLoS One. 2010 Aug 5;5(8):e11980.
Sinclair MS, Perea-Martinez I, Dvoryanchikov G, Yoshida M, Nishimori K, Roper SD, Chaudhari N.
Program in Neurosciences, Department of Physiology & Biophysics, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
Oxytocin (OXT), a nonapeptide hormone classically known to facilitate lactation and parturition, is also a central neuropeptide that influences a host of social and other behaviors. The peripheral actions of OXT are elicited principally following its release into the bloodstream from hypothalamic magnocellular neurons with terminals in the pituitary. The central effects of OXT are in response to release from magnocellular dendrites and axonal projections of parvocellular neurons
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0011980
Ghrelin is produced in taste cells and ghrelin receptor null mice show reduced taste responsivity to salty (NaCl) and sour (citric acid) tastants
PLoS One. 2010 Sep 14;5(9):e12729.
Shin YK, Martin B, Kim W, White CM, Ji S, Sun Y, Smith RG, Sévigny J, Tschöp MH, Maudsley S, Egan JM.
National Institute on Aging/National Institutes of Health, Baltimore, Maryland, United States of America. Abstract BACKGROUND: The gustatory system plays a critical role in determining food preferences, food intake and energy balance. The exact mechanisms that fine tune taste sensitivity are currently poorly defined, but it is clear that numerous factors such as efferent input and specific signal transduction cascades are involved.
METHODOLOGY/PRINCIPAL FINDINGS: Using immunohistochemical analyses, we show that ghrelin, a hormone classically considered to be an appetite-regulating hormone, is present within the taste buds of the tongue. Prepro-ghrelin, prohormone convertase 1/3 (PC 1/3), ghrelin, its cognate receptor (GHSR), and ghrelin-O-acyltransferase (GOAT , the enzyme that activates ghrelin) are expressed in Type I, II, III and IV taste cells of mouse taste buds. In addition, ghrelin and GHSR co-localize in the same taste cells, suggesting that ghrelin works in an autocrine manner in taste cells. To determine a role for ghrelin in modifying taste perception, we performed taste behavioral tests using GHSR null mice. GHSR null mice exhibited significantly reduced taste responsivity to sour (citric acid) and salty (sodium chloride) tastants.
CONCLUSIONS/SIGNIFICANCE: These findings suggest that ghrelin plays a local modulatory role in determining taste bud signaling and function and could be a novel mechanism for the modulation of salty and sour taste responsivity.
PMID 20856820
Evidence for a role of glutamate as an efferent transmitter in taste buds
Vandenbeuch A, Tizzano M, Anderson CB, Stone LM, Goldberg D, Kinnamon SC. BMC Neurosci. 2010 Jun 21;11:77.
BACKGROUND: Glutamate has been proposed as a transmitter in the peripheral taste system in addition to its well-documented role as an umami taste stimulus. Evidence for a role as a transmitter includes the presence of ionotropic glutamate receptors in nerve fibers and taste cells, as well as the expression of the glutamate transporter GLAST in Type I taste cells. However, the source and targets of glutamate in lingual tissue are unclear. In the present study, we used molecular, physiological and immunohistochemical methods to investigate the origin of glutamate as well as the targeted receptors in taste buds.
RESULTS: Using molecular and immunohistochemical techniques, we show that the vesicular transporters for glutamate, VGLUT 1 and 2, but not VGLUT3, are expressed in the nerve fibers surrounding taste buds but likely not in taste cells themselves. Further, we show that P2X2, a specific marker for gustatory but not trigeminal fibers, co-localizes with VGLUT2, suggesting the VGLUT-expressing nerve fibers are of gustatory origin. Calcium imaging indicates that GAD67-GFP Type III taste cells, but not T1R3-GFP Type II cells, respond to glutamate at concentrations expected for a glutamate transmitter, and further, that these responses are partially blocked by NBQX, a specific AMPA/Kainate receptor antagonist. RT-PCR and immunohistochemistry confirm the presence of the Kainate receptor GluR7 in Type III taste cells, suggesting it may be a target of glutamate released from gustatory nerve fibers.
CONCLUSIONS: Taken together, the results suggest that glutamate may be released from gustatory nerve fibers using a vesicular mechanism to modulate Type III taste cells via GluR7.
PMID 20565975
2009
Genome-wide analysis of gene expression in primate taste buds reveals links to diverse processes
PLoS One. 2009 Jul 28;4(7):e6395.
Hevezi P, Moyer BD, Lu M, Gao N, White E, Echeverri F, Kalabat D, Soto H, Laita B, Li C, Yeh SA, Zoller M, Zlotnik A.
Senomyx, Inc, San Diego, California, United States of America. Abstract Efforts to unravel the mechanisms underlying taste sensation (gustation) have largely focused on rodents. Here we present the first comprehensive characterization of gene expression in primate taste buds. Our findings reveal unique new insights into the biology of taste buds. We generated a taste bud gene expression database using laser capture microdissection (LCM) procured fungiform (FG) and circumvallate (CV) taste buds from primates. We also used LCM to collect the top and bottom portions of CV taste buds. Affymetrix genome wide arrays were used to analyze gene expression in all samples. Known taste receptors are preferentially expressed in the top portion of taste buds. Genes associated with the cell cycle and stem cells are preferentially expressed in the bottom portion of taste buds, suggesting that precursor cells are located there. Several chemokines including CXCL14 and CXCL8 are among the highest expressed genes in taste buds, indicating that immune system related processes are active in taste buds. Several genes expressed specifically in endocrine glands including growth hormone releasing hormone and its receptor are also strongly expressed in taste buds, suggesting a link between metabolism and taste. Cell type-specific expression of transcription factors and signaling molecules involved in cell fate, including KIT, reveals the taste bud as an active site of cell regeneration, differentiation, and development. IKBKAP, a gene mutated in familial dysautonomia, a disease that results in loss of taste buds, is expressed in taste cells that communicate with afferent nerve fibers via synaptic transmission. This database highlights the power of LCM coupled with transcriptional profiling to dissect the molecular composition of normal tissues, represents the most comprehensive molecular analysis of primate taste buds to date, and provides a foundation for further studies in diverse aspects of taste biology.
PMID 19636377
Fate mapping of mammalian embryonic taste bud progenitors
Thirumangalathu S, Harlow DE, Driskell AL, Krimm RF, Barlow LA. Development. 2009 May;136(9):1519-28. PMID 19363153
In mammals, the homogeneous lingual epithelium in the process of development forms specialized placodal cells that undergo a series of morphogenetic changes to form a papilla. Taste buds appear in the papillary epithelium around birth and thus papillae serve to house the taste buds in the adult. However, evidence for a precise lineage relationship between a putative embryonic taste progenitor population and functional adult taste buds has so far been elusive and is primarily indirect. Also, mammalian taste papillae are reminiscent of epithelial appendages suggesting that the mesenchymal tissue of the papillae could be involved in the formation of these lingual structures. These major questions in the field of mammalian taste development have remained unanswered due to lack of fate mapping studies that would label embryonic cell populations and remain indelibly marked in the adult. Taking advantage of a genetic fate mapping approach to label cell populations both in the lingual epithelium and mesenchyme and following their fate during development would be an ideal way to assess each of these tissues contribution in taste bud formation. Fate mapping studies using tissue specific cre strains crossed with reporter alleles would uncover unique features in the formation of these specialized sensory cells and also provide us with an in vivo model system for taste organ specific experimental manipulations during development.
Inflammation and taste disorders: mechanisms in taste buds
Ann N Y Acad Sci. 2009 Jul;1170:596-603.
Wang H, Zhou M, Brand J, Huang L.
Monell Chemical Senses Center, Philadelphia, Pennsylvania 19104, USA. hwang@monell.org Abstract Taste disorders, including taste distortion and taste loss, negatively impact general health and quality of life. To understand the underlying molecular and cellular mechanisms, we set out to identify inflammation-related molecules in taste tissue and to assess their role in the development of taste dysfunctions. We found that 10 out of 12 mammalian Toll-like receptors (TLRs), type I and II interferon (IFN) receptors, and their downstream signaling components are present in taste tissue. Some TLRs appear to be selectively or more abundantly expressed in taste buds than in nongustatory lingual epithelium. Immunohistochemistry with antibodies against TLRs 1, 2, 3, 4, 6, and 7 confirmed the presence of these receptor proteins in taste bud cells, of which TLRs 2, 3, and 4 are expressed in the gustducin-expressing type II taste bud cells. Administration of TLR ligands, lipopolysaccharide, and double-stranded RNA polyinosinic:polycytidylic acid, which mimics bacterial or viral infection, activates the IFN signaling pathways, upregulates the expression of IFN-inducible genes, and downregulates the expression of c-fos in taste buds. Finally, systemic administration of IFNs augments apoptosis of taste bud cells in mice. Taken together, these data suggest that TLR and IFN pathways function collaboratively in recognizing pathogens and mediating inflammatory responses in taste tissue. This process, however, may interfere with normal taste transduction and taste bud cell turnover and contributes to the development of taste disorders.
PMID 19686199
The rostral migratory stream and olfactory system: smell, disease and slippery cells
Prog Brain Res. 2009;175:33-42.
Curtis MA, Monzo HJ, Faull RL.
Department of Anatomy with Radiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. m.curtis@auckland.ac.nz Abstract In the mammalian brain, olfaction is an important sense that is used to detect odors of different kinds that can warn of off food, to produce a mothering instinct in a flock or group of animals, and to warn of danger such as fire or poison. The olfactory system is made up of a long-distance rostral migratory stream that arises from the subventricular zone in the wall of the lateral ventricle, mainly comprises neuroblasts, and stretches all the way through the basal forebrain to terminate in the olfactory bulb. The olfactory bulb receives a constant supply of new neurons that allow ongoing integration of new and different smells, and these are integrated into either the granule cell layer or the periglomerular layer. The continuous turnover of neurons in the olfactory bulb allows us to study the proliferation, migration, and differentiation of neurons and their application in therapies for neurodegenerative diseases. In this chapter, we will examine the notion that the olfactory system might be the route of entry for factors that cause or contribute to neurodegeneration in the central nervous system. We will also discuss the enzymes that may be involved in the addition of polysialic acid to neural cell adhesion molecule, which is vital for allowing the neuroblasts to move through the rostral migratory stream. Finally, we will discuss a possible role of endosialidases for removing polysialic acid from neural cell adhesion molecules, which causes neuroblasts to stop migrating and terminally differentiate into olfactory bulb interneurons.
PMID 19660647
2007
Embryonic origin of gustatory cranial sensory neurons
Dev Biol. 2007 Oct 15;310(2):317-28. Epub 2007 Aug 15.
Harlow DE, Barlow LA.
Department of Cell and Developmental Biology, Rocky Mountain Taste and Smell Center, University of Colorado Denver Health Sciences Center, Anschutz Medical Campus, Aurora, CO 80045, USA. danielle.harlow@uchsc.edu Abstract Cranial nerves VII, IX and X provide both gustatory (taste) and non-gustatory (touch, pain, temperature) innervation to the oral cavity of vertebrates. Gustatory neurons innervate taste buds and project centrally to the rostral nucleus of the solitary tract (NTS), whereas neurons providing general epithelial innervation to the oropharynx project to non-gustatory hindbrain regions, i.e., spinal trigeminal nucleus. In addition to this dichotomy in function, cranial ganglia VII, IX and X have dual embryonic origins, comprising sensory neurons derived from both cranial neural crest and epibranchial placodes. We used a fate mapping approach to test the hypothesis that epibranchial placodes give rise to gustatory neurons, whereas the neural crest generates non-gustatory cells. Placodal ectoderm or neural crest was grafted from Green Fluorescent Protein (GFP) expressing salamander embryos into unlabeled hosts, allowing us to discern the postembryonic central and peripheral projections of each embryonic neuronal population. Neurites that innervate taste buds are exclusively placodal in origin, and their central processes project to the NTS, consistent with a gustatory fate. In contrast, neural crest-derived neurons do not innervate taste buds; instead, neurites of these sensory neurons terminate as free nerve endings within the oral epithelium. Further, the majority of centrally directed fibers of neural crest neurons terminate outside the NTS, in regions that receive general epithelial afferents. Our data provide empirical evidence that embryonic origin dictates mature neuron function within cranial sensory ganglia: specifically, gustatory neurons derive from epibranchial placodes, whereas neural crest-derived neurons provide general epithelial innervation to the oral cavity.
PMID 17826760
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836672
1996
Embryonic and early fetal development of human taste buds: a transmission electron microscopical study
Anat Rec. 1996 Dec;246(4):507-23.
Witt M, Reutter K. Source Department of Anatomy, Technical University Dresden, Germany.
Abstract
BACKGROUND: Taste buds are assemblies of slender epithelial cells that receive chemical stimuli from the outer (oral) environment. In contrast to the large and well documented information on the morphology of taste buds in adult humans and animals, there are only a few reports on fetal ones, and ultrastructural studies of prenatal human taste buds are lacking completely. Therefore, the present investigation has been carried out to study the taste bud primordium, its morphological changes including synaptogenesis, cell differentiation, and taste pore formation from the time of the onset of taste bud formation around the 8th week until the 15th postovulatory week. METHODS: Taste bud primordia of 42 human embryonic/fetal tongues have been examined by means of transmission electron microscopy. RESULTS: Nerve fibers approach the lingual epithelium between the 6th and 7th postovulatory week. They penetrate the basal lamina during the 8th week and form synapses with poorly differentiated, elongated, epithelial cells. By the 12th week, more differentiated cell types are seen: 1) electron-dense cells resembling type III cells of the adult taste bud containing large numbers of dense-cored vesicles (80-150 nm in diameter); 2) electron-dark cells with well developed endoplasmic reticulum and many apical mitochondria, being candidates for type II cells. Basally, these cells have foot-like processes containing dense-cored vesicles (120-200 nm in diameter), but they do not synapse to nerve fibers. Type I cells, characterized by apically located dense secretory granules, are not observed. First shallow grooves above the taste bud primordium are found around the 10th week. Untypically differentiated apical cellular processes extend onto the surface. Most of the taste pores develop around the 14th to 15th week. In the taste pit, mucous material is not present during the first 15 weeks of gestation. Synapses between cells and afferent nerve fibers were found by the 8th week, reaching a maximum around the 12th to 13th week. CONCLUSIONS: The early presence of taste bud cells containing dense-cored vesicles suggests an at least dual function of embryonic/ fetal taste buds: First, from the 8th until the 14th week, non-gustatory, paracrine functions should be considered. After the 14th week of gestation, when typical taste pores are present, the taste buds possibly start their gustatory function. Differentiated marginal cells are possibly involved in the formation of the taste pore. The lack of type I cells producing the mucous material in the taste pit indicates that the taste bud has not achieved a fully developed function until the 15th week of gestation.
PMID 8955790
Book Ref
Mistretta CM. Developmental Neurobiology of taste. In: Getchell T DR, Bartoshuk L, Snow J, editors. Smell and Taste in Health and Disease. Raven Press; New York: 1991. pp. 35–64.
GIT
Introduction to Salivary Glands: Structure, Function and Embryonic Development. Miletich I. Front Oral Biol. 2010;14:1-20. Epub 2010 Apr 20. PMID: 20428008
- "Salivary glands are a group of organs secreting a watery substance that is of utmost importance for several physiological functions ranging from the protection of teeth and surrounding soft tissues to the lubrication of the oral cavity, which is crucial for speech and perception of food taste. Salivary glands are complex networks of hollow tubes and secretory units that are found in specific locations of the mouth and which, although architecturally similar, exhibit individual specificities according to their location. This chapter focuses on the embryonic development of vertebrate salivary glands, which has been classically studied in the mouse model system since the 1950s. We describe here where, when and how major salivary glands develop in the lower jaw of the mouse embryo. Key mechanisms involved in this process are discussed, including reciprocal tissue interactions between epithelial and mesenchymal cells, epithelial branching morphogenesis and coordinated cell deathand cell proliferation. Copyright © 2010 S. Karger AG, Basel."
- "In mammals, the homogeneous lingual epithelium in the process of development forms specialized placodal cells that undergo a series of morphogenetic changes to form a papilla. Taste buds appear in the papillary epithelium around birth and thus papillae serve to house the taste buds in the adult."[1]
Factors that regulate embryonic gustatory development http://www.biomedcentral.com/1471-2202/8/S3/S4
- ↑ <pubmed>19686103</pubmed>
