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Recently, the transient receptor potential vanilloid type 1 (TRPV1) channel was shown to be involved in capacitation, the process that allows mammalian spermatozoa to acquire their fertilizing ability within the female genital tract. Unfortunately, the role of TRPV1 in this process is still unclear. Thus, the aims of the present work were to 1) investigate the function of TRPV1 in the male gamete signaling system and 2) modulate TRPV1 activity by administering a specific activator, capsaicin, or a specific inhibitor, capsazepin, to spermatozoa during in vitro capacitation. Using confocal microscopy, cellular responses were assessed in terms of changes in 1) cell membrane resting potential, 2) intracellular calcium concentrations, and 3) actin polymerization dynamics. As a result, TRPV1 channels were shown to act as specific cationic channels: their activation led to membrane depolarization and, consequently, the opening of voltage-gated calcium channels and an increase in intracellular calcium concentrations. These ionic events promote actin cytoskeletal depolymerization and a loss of acrosome structure integrity. In contrast, TRPV1 inhibition caused a slowing of the capacitation-dependent increase in intracellular calcium concentrations, a reduction in actin polymerization, and acrosome rupture. In conclusion, these results suggest that TRPV1 channels modulate the major pathways involved in capacitation.

Role of TRPV1 channels during the acquisition of fertilizing ability in boar spermatozoa