Department of Biology, Faculty of Education and Integrated Sciences, Waseda University, Tokyo 169-8050, Japan.
Peptides. 2013 Jul;45:15-21. doi: 10.1016/j.peptides.2013.04.006. Epub 2013 Apr 22.
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.
一种叫做 sodefrin 的红腹雄性蝾螈的肽类信息素,通过钙离子成像系统检测其在雌性离体犁鼻器(VN)细胞中增加细胞内钙离子浓度([Ca2+]i)的能力。该信息素可引起性成熟雌性 VN 细胞中一小部分细胞的[Ca2+]i 显著升高。表现出 sodefrin 诱导[Ca2+]i 升高的细胞群体呈浓度依赖性增加。在这方面,不同物种的信息素是无效的。来自非繁殖期雌性或繁殖期雄性的 VN 细胞在提高[Ca2+]i 方面几乎对 sodefrin 没有反应。在垂体切除和卵巢切除的雌性细胞中,sodefrin 诱导的[Ca2+]i 增加从未发生过。在接受催乳素和雌二醇补充的手术蝾螈细胞中,sodefrin 诱导的[Ca2+]i 反应具有高发生率。因此,VN 细胞对 sodefrin 的反应在细胞水平上表现出性别和激素依赖性以及物种特异性。随后,使用药理学方法探讨了 PLC-肌醇 1,4,5-三磷酸(IP3)和/或 PLC-二酰基甘油(DAG)-蛋白激酶 C(PKC)途径参与 sodefrin 增加 VN 细胞[Ca2+]i 的可能性。结果表明,PLC 参与了所有 sodefrin 反应性 VN 细胞中 Ca2+信号的产生,而 IP3 参与了大约 50%的细胞,DAG-PKC 参与了其余细胞。在后一种情况下,通过 L 型通道的钙内流假设引起[Ca2+]i 的增加。讨论了该发现的意义。