title: Oxytocin signaling in mouse taste buds.
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.
  
  
  RESULTS
  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 approximately 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
  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.
authors.affiliation: Program in Neurosciences, Department of Physiology & Biophysics, University of Miami Miller School of Medicine, Miami, Florida, United States of America.
authors.forename: Michael S
authors.initials: MS
authors.lastname: Sinclair
authors.forename: Isabel
authors.initials: I
authors.lastname: Perea-Martinez
authors.forename: Gennady
authors.initials: G
authors.lastname: Dvoryanchikov
authors.forename: Masahide
authors.initials: M
authors.lastname: Yoshida
authors.forename: Katsuhiko
authors.initials: K
authors.lastname: Nishimori
authors.forename: Stephen D
authors.initials: SD
authors.lastname: Roper
authors.forename: Nirupa
authors.initials: N
authors.lastname: Chaudhari
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004435:Eating; D005786:Gene Expression Regulation; D055879:Gene Knock-In Techniques; D051379:Mice; D008822:Mice, Transgenic; D009457:Neuroglia / Q000166:cytology; D010121:Oxytocin / Q000378:metabolism* / Q000494:pharmacology; D018045:Receptors, Oxytocin / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D013650:Taste Buds / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*
chemical_list: D018045:Receptors, Oxytocin; D010121:Oxytocin; D002118:Calcium