Talk:Sensory - Taste Development: Difference between revisions

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PMID: 20856820
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
http://www.ncbi.nlm.nih.gov/pubmed/20565975


==2009==
==2009==

Revision as of 15:20, 23 November 2010

2010

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 http://www.ncbi.nlm.nih.gov/pubmed/20565975

2009

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

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/?tool=pubmed

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

  1. <pubmed>19686103</pubmed>