Oxytocin signaling in mouse taste buds

Michael S. Sinclair, Isabel Perea-Martinez, Gennady Dvoryanchikov, Masahide Yoshida, Katsuhiko Nishimori, Stephen D Roper, Nirupa Chaudhari

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Background: The neuropeptide, oxytocin (OXT), acts on brain circuits to inhibit food intake. Mutant mice lacking OXT (OXT knockout) overconsume salty and sweet (i.e. sucrose, saccharin) solutions. We asked if OXT might also act on taste buds via its receptor, OXTR. Methodology/Principal Findings: Using RT-PCR, we detected the expression of OXTR in taste buds throughout the oral cavity, but not in adjacent non-taste lingual epithelium. By immunostaining tissues from OXTR-YFP knock-in mice, we found that OXTR is expressed in a subset of Glial-like (Type I) taste cells, and also in cells on the periphery of taste buds. Single-cell RT-PCR confirmed this cell-type assignment. Using Ca2+ imaging, we observed that physiologically appropriate concentrations of OXT evoked [Ca2+]i mobilization in a subset of taste cells (EC50, 33 nM). OXT-evoked responses were significantly inhibited by the OXTR antagonist, L-371,257. Isolated OXT-responsive taste cells were neither Receptor (Type II) nor Presynaptic (Type III) cells, consistent with our immunofluorescence observations. We also investigated the source of OXT peptide that may act on taste cells. Both RT-PCR and immunostaining suggest that the OXT peptide is not produced in taste buds or in their associated nerves. Finally, we also examined the morphology of taste buds from mice that lack OXTR. Taste buds and their constituent cell types appeared very similar in mice with two, one or no copies of the OXTR gene. Conclusions/Significance: We conclude that OXT elicits Ca2+ signals via OXTR in murine taste buds. OXT-responsive cells are most likely a subset of Glial-like (Type I) taste cells. OXT itself is not produced locally in taste tissue and is likely delivered through the circulation. Loss of OXTR does not grossly alter the morphology of any of the cell types contained in taste buds. Instead, we speculate that OXT-responsive Glial-like (Type I) taste bud cells modulate taste signaling and afferent sensory output. Such modulation would complement central pathways of appetite regulation that employ circulating homeostatic and satiety signals.

Original languageEnglish
Article numbere11980
JournalPLoS One
Volume5
Issue number8
DOIs
StatePublished - Oct 15 2010

Fingerprint

Taste Buds
oxytocin
palps
Oxytocin
mice
cells
neuroglia
Neuroglia
reverse transcriptase polymerase chain reaction
L 371257
calcium
Polymerase Chain Reaction
peptides
Tissue
Appetite Regulation
saccharin
Saccharin
Peptides
receptors
neuropeptides

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Sinclair, M. S., Perea-Martinez, I., Dvoryanchikov, G., Yoshida, M., Nishimori, K., Roper, S. D., & Chaudhari, N. (2010). Oxytocin signaling in mouse taste buds. PLoS One, 5(8), [e11980]. https://doi.org/10.1371/journal.pone.0011980

Oxytocin signaling in mouse taste buds. / Sinclair, Michael S.; Perea-Martinez, Isabel; Dvoryanchikov, Gennady; Yoshida, Masahide; Nishimori, Katsuhiko; Roper, Stephen D; Chaudhari, Nirupa.

In: PLoS One, Vol. 5, No. 8, e11980, 15.10.2010.

Research output: Contribution to journalArticle

Sinclair, MS, Perea-Martinez, I, Dvoryanchikov, G, Yoshida, M, Nishimori, K, Roper, SD & Chaudhari, N 2010, 'Oxytocin signaling in mouse taste buds', PLoS One, vol. 5, no. 8, e11980. https://doi.org/10.1371/journal.pone.0011980
Sinclair MS, Perea-Martinez I, Dvoryanchikov G, Yoshida M, Nishimori K, Roper SD et al. Oxytocin signaling in mouse taste buds. PLoS One. 2010 Oct 15;5(8). e11980. https://doi.org/10.1371/journal.pone.0011980
Sinclair, Michael S. ; Perea-Martinez, Isabel ; Dvoryanchikov, Gennady ; Yoshida, Masahide ; Nishimori, Katsuhiko ; Roper, Stephen D ; Chaudhari, Nirupa. / Oxytocin signaling in mouse taste buds. In: PLoS One. 2010 ; Vol. 5, No. 8.
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