title: Responsiveness of vomeronasal cells to a newt peptide pheromone, sodefrin as monitored by changes of intracellular calcium concentrations.
abstract: A peptide pheromone of the red-bellied male newt, sodefrin was tested for its ability to increase intracellular concentrations of Ca(2+) ([Ca(2+)]i) in the dissociated vomeronasal (VN) cells of females by means of calcium imaging system. The pheromone elicited a marked elevation of [Ca(2+)]i in a small population of VN cells from sexually developed females. The population of cells exhibiting sodefrin-induced elevation of [Ca(2+)]i increased concentration-dependently. A pheromone of a different species was ineffective in this respect. The VN cells from non-reproductive females or from reproductive males scarcely responded to sodefrin in terms of elevating [Ca(2+)]i. In the cells from hypophysectomized and ovariectomized females, the sodefrin-inducible increase of [Ca(2+)]i never occurred. The cells from the operated newts supplemented with prolactin and estradiol exhibited [Ca(2+)]i responses to sodefrin with a high incidence. Thus, sex- and hormone-dependency as well as species-specificity of the responsiveness of the VN cells to sodefrin was evidenced at the cellular level. Subsequently, possibility of involvement of phospholipase C (PLC)-inositol 1,4,5-trisphosphate (IP3) and/or PLC-diacylglycerol (DAG)-protein kinase C (PKC) pathways in increasing [Ca(2+)]i in VN cells in response to sodefrin was explored using pharmacological approaches. The results indicated that PLC is involved in generating the Ca(2+) signal in all sodefrin-responsive VN cells, whereas IP3 in approximately 50% of the cells and DAG-PKC in the remaining cells. In the latter case, the increase of [Ca(2+)]i was postulated to be induced by the influx of Ca(2+) through the L-type channel. The significance of the finding is discussed.
authors.affiliation: Department of Biology, Faculty of Education and Integrated Sciences, Waseda University, Tokyo 169-8050, Japan.
authors.forename: Takeo
authors.initials: T
authors.lastname: Iwata
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Nakada
authors.forename: Fumiyo
authors.initials: F
authors.lastname: Toyoda
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Yada
authors.forename: Seiji
authors.initials: S
authors.lastname: Shioda
authors.forename: Sakae
authors.initials: S
authors.lastname: Kikuyama
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling; D049109:Cell Proliferation; D004075:Diglycerides / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D007016:Hypophysectomy; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D008297:Male; D057054:Molecular Imaging; D009842:Oligopeptides / Q000494:pharmacology*; D010052:Ovariectomy; D010053:Ovary / Q000502:physiology; D010902:Pituitary Gland / Q000502:physiology; D061251:Primary Cell Culture; D011388:Prolactin / Q000494:pharmacology; D011493:Protein Kinase C / Q000378:metabolism; D012455:Salamandridae / Q000502:physiology*; D012724:Sex Attractants / Q000494:pharmacology*; D012726:Sexual Behavior, Animal / Q000502:physiology*; D013045:Species Specificity; D019147:Vomeronasal Organ / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism
chemical_list: C011439:1,2-diacylglycerol; D004075:Diglycerides; D009842:Oligopeptides; D012724:Sex Attractants; C092479:sodefrin; D004958:Estradiol; D015544:Inositol 1,4,5-Trisphosphate; D011388:Prolactin; D011493:Protein Kinase C; D002118:Calcium