Molecular mechanisms of mammalian sperm capacitation, and its regulation by sodium-dependent secondary active transporters.

Abstract

Mammalian spermatozoa have to be "capacitated" to be fertilization-competent. Capacitation is a collective term for the physiological and biochemical changes in spermatozoa that occur within the female body. However, the regulatory mechanisms underlying capacitation have not been fully elucidated. Previously published papers on capacitation, especially from the perspective of ions/channels/transporters, were extracted and summarized. Capacitation can be divided into two processes: earlier events (membrane potential hyperpolarization, intracellular pH rise, intracellular Ca2+ rise, etc.) and two major later events: hyperactivation and the acrosome reaction. Earlier events are closely interconnected with each other. Various channels/transporters are involved in the regulation of them, which ultimately lead to the later events. Manipulating the extracellular K+ concentration based on the oviductal concentration modifies membrane potential; however, the later events and fertilization are not affected, suggesting the uninvolvement of membrane potential in capacitation. Hyperpolarization is a highly conserved phenomenon among mammalian species, indicating its importance in capacitation. Therefore, the physiological importance of hyperpolarization apart from membrane potential is suggested. The hypotheses are (1) hyperpolarizing Na+ dynamics (decrease in intracellular Na+) and Na+-driven secondary active transporters play a vital role in capacitation and (2) the sperm-specific potassium channel Slo3 is involved in volume and/or morphological regulation.