Role of Ca(2+) and Calmodulin on the Initiation of Sperm Motility in Salmonid Fishes

• Published in: Journal of microbiology and biotechnology Vol. 14; no. 3; pp. 456 - 465
• Main Authors: Kho, Kang-Hee, Morisawa, Masaaki, Choi, Kap-Seong
• Format: Journal Article
• Language: Korean
• Published: 한국미생물생명공학회 30.06.2004
• Subjects: Ca(2+) ion channel; calmodulin; Sperm motility; calmodulin; Sperm motility; Ca^{2+}$ ion channel
• ISSN: 1017-7825; 1738-8872

$K^+$ efflux through a certain type of $K^+$ channels causes the change of membrane potential and leads to cAMP synthesis in the transmembrane cell signaling for the initiation of sperm motility in the salmonid fishes. The addition of $Ca^{2+}$ conferred motility to the trout sperm that were immobilized by external $K^+$ and other alkaline metals, $Rb^+$ and $Cs^{2+}$, suggesting the participation of external $Ca^{2+}$ in the initiation of sperm motility. L-type $Ca^{2+}$ channel blockers such as nifedipine, nimodipine, and FS-2 inhibited the motility, but N-type $Ca^{2+}$ channel blocker, w-conotoxin MvIIA, did not. On the other hand, the membrane hyperpolarization and cAMP synthesis were suppressed by $Ca^{2+}$ channel blockers, nifedipine, and trifluoroperazine. Furthermore, these suppressions were relieved by the addition of $K^+$ ionophore, valinomycin. Inhibitors of calmodulin, such as W-7, trifluoperazine, and calrnidazol-C1, inhibited the sperm motility, membrane hyperpolarization, and cAMP synthesis. The results suggest that $Ca^{2+}$ influx through $Ca^{2+}$ channels that are sensitive to specific $Ca^{2+}$ channel blockers and calmodulin participate in the changes of membrane potential, leading to synthesis of cAMP in the cell signaling for the initiation of trout sperm motility.