Physiological functions of osmolality and calcium ions on the initiation of sperm motility and swimming performance in redside dace, Clinostomus elongatus.

Reproductive potential of fish stocks is critically dependent on sperm performance in an aquatic environment. The aim of this study is to test hypotheses, which govern the initiation of sperm motility and swimming performance, through physiological functions of osmolality and Ca(2+) ion, in a threatened species of freshwater fish, the redside dace, Clinostomus elongatus. Spermatozoa motility was activated in either ionic or non-ionic media spanning a range of osmolalities. The role of Ca(2+) channels on induction of spermatozoa motility and velocity was experimentally investigated by diluting sperm in media that contain various Ca(2+) channel blockers. Results show that initiation of spermatozoa motility is a hypo-osmolality dependent mechanism. Inhibitors for L-type Ca(2+) channels partially prohibited initiation of spermatozoa motility, while velocity was significantly reduced in both L-type and T-type Ca(2+) channel blockers. Examination using W-7, an inhibitor for Ca(2+)-dependent calmodulin, showed significant decreases in spermatozoa motility and velocity. Involvement for Ca(2+) in axonemal beating was confirmed by significant increases in velocity after adding Ca(2+) into the activation media, while motility remained unchanged in Ca(2+) supplemented activation media. Together, these findings suggest the involvement of Ca(2+) in hypo-osmolality-dependent initiation of spermatozoa motility mediated by activation of Ca(2+) binding protein in the axoneme of a freshwater fish sperm. Blocking Ca(2+) exchange through L- or T-type Ca(2+) channel influences flagellar beating force and leads to decrease in spermatozoa velocity.