Department of Biochemistry, Showa University School of Medicine, 1-5-8, Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; Center for Advanced Biomedical Sciences, Research Institute for Science and Engineering, Waseda University, 2-2, Wakamatsu-cho, Shinjuku-ku, Tokyo 162-8480, Japan.
Bioorganic Research Institute, Suntory Foundation for Life Sciences, 8-1-1 Seikadai, Seika-cho, Soraku-gun, Kyoto 619-0284, Japan.
Gen Comp Endocrinol. 2020 May 1;290:113401. doi: 10.1016/j.ygcen.2020.113401. Epub 2020 Jan 22.
Starfish are suitable animals for the study of hormonal regulatory mechanism of oocyte maturation and ovulation. Although contraction of the gonadal walls is essential for the shedding gametes, little was known about the mechanism. When ovaries of starfish Patiria pectinifera were incubated in Ca-free seawater in the presence of 1-methyladenine (1-MeAde), the germinal vesicles in oocytes broke down, but no ovulation occurred. Verapamil, a potent inhibitor of voltage-dependent Ca channels, inhibited 1-MeAde-induced ovulation. These results suggest that extracellular Ca and its influx are indispensable for gamete shedding. Furthermore, acetylcholine (ACh) was involved in extracellular Ca-dependent contractions of gonadal walls. Although 1-MeAde failed to induce contraction of the gonadal walls in normal seawater containing L-glutamic acid, application of ACh or carbachol, an agonist for ACh receptor, could bring about shedding of mature oocytes. Atropine, a competitive antagonist of the muscarinic ACh receptor, inhibited 1-MeAde-induced ovulation, but a nicotinic ACh receptor antagonist mecamylamine had no effect. Furthermore, ACh was detected in the ovaries and testes in P. pectinifera. These findings suggest that ACh acts on muscarinic ACh receptors in gonadal walls to induce peristaltic contractions caused by Ca influx via Ca channels in the gonadal wall muscle for gamete shedding. The present study also provides new insight into the regulatory mechanism that 1-MeAde acts on secretion of ACh in ovaries and testes.
海星是研究卵母细胞成熟和排卵的激素调节机制的合适动物。尽管性腺壁的收缩对于释放配子是必不可少的，但对于其机制却知之甚少。当星鱼 Patiria pectinifera 的卵巢在含有 1-甲基腺嘌呤（1-MeAde）的无钙海水中孵育时，卵母细胞中的生殖泡破裂，但没有排卵发生。维拉帕米是电压依赖性钙通道的有效抑制剂，它抑制了 1-MeAde 诱导的排卵。这些结果表明细胞外钙及其内流对于配子的释放是不可或缺的。此外，乙酰胆碱（ACh）参与了性腺壁的细胞外钙依赖性收缩。尽管 1-MeAde 未能在含有 L-谷氨酸的正常海水中诱导性腺壁的收缩，但应用 ACh 或 carbachol（ACh 受体的激动剂）可以导致成熟卵母细胞的释放。阿托品是毒蕈碱型 ACh 受体的竞争性拮抗剂，它抑制了 1-MeAde 诱导的排卵，但烟碱型 ACh 受体拮抗剂 mecamylamine 没有影响。此外，在 P.pectinifera 的卵巢和睾丸中检测到了 ACh。这些发现表明，ACh 作用于性腺壁上的毒蕈碱型 ACh 受体，通过钙通道引起钙内流，从而引发蠕动收缩，导致配子的释放。本研究还为 1-MeAde 作用于卵巢和睾丸中 ACh 分泌的调节机制提供了新的见解。
