Regulation of mammalian sperm motility

The physiological regulation of sperm motility has become more amendable to investigation since the demonstration that cAMP and calcium play a role in modulating the functioning of the flagellar axoneme. Although the external triggering mechanisms that initiate motility and capacitation are still unknown, evidence supports a modification of the calcium balance by gated Ca2+ channels, accompanied by shifts in the internal pH. Ca2+ and pH may in turn act indirectly through cAMP and cAMP-dependent kinase (kinase(a] to control the phosphorylation state of functional proteins in the flagellar axoneme. The role of calcium is of central importance, but it is clear that several separate Ca2+-dependent mechanisms are involved. Ca2+ controls the curvature of the sperm flagellum and, so, can change the motility of the sperm from progressive swimming to tumbling. Under the appropriate conditions, calcium appears to have the capacity to deactivate motility by activating phosphodiesterase and phosphatase. The deactivating effect of Ca2+ may be offset under some circumstances by coactivation of adenyl cyclase, so phosphorylation of the axoneme and the motility are maintained. The specific factors determining the predominant calcium effect are not yet known, but internal pH of the sperm may play a major role.