Figure 1.

Immediately after ejaculation (early events) TRPV1 receptors are located in post-equatorial area and are functionally inactive (1). The slowly increasing [Ca²⁺]_i allows G-actin polymerization, thus creating a diaphragm between PM and OAM (2). cAMP concentration is maintained at a low level by CB₁ located in the post-equatorial area, which actively inhibits tmAC, and by a low intracellular concentration of bicarbonate (A). Progressively (late events) TRPV1 translocates in the acrosomal area and becomes active (1). Its opening triggers a membrane depolarization wave (2) and, as a consequence, the recruitment of VOCCs which, in turn, promote a dramatic increase in [Ca²⁺]_i (3). The latter event causes a fast depolymerization of F-actin network (4), thus allowing the contact between PM and OAM. At the same time, CB₁ migrates in the equatorial area and becomes inactive (A). This event, along with the markedly increased intracellular concentration of bicarbonate (B), promotes the rise in cAMP levels (C) that, via a PKA-dependent pathway, causes the activation of lipid scrambling and increases membrane fusogenicity (D).