Expression, localization and functions in acrosome reaction and sperm motility of ca(v)3.1 and ca(v)3.2 channels in sperm cells: an evaluation from ca(v)3.1 and ca(v)3.2 deficient mice

Abstract

In spermatozoa, voltage-dependent calcium channels (VDCC) have been involved in different cellular functions like acrosome reaction (AR) and sperm motility. Multiple types of VDCC are present and their relative contribution is still a matter of debate. Based mostly on pharmacological studies, Low-Voltage-Activated Calcium Channels (LVA-CC), responsible of the inward current in spermatocytes, were described as essential for AIR in sperm. The development of Ca(v)3.1 or Ca(v)3.2 null mice provided the opportunity to evaluate the involvement of such LVA-CC in AIR and sperm motility, independently of pharmacological tools. The inward current was fully abolished in spermatogenic cells from Cav3.2 deficient mice. This current is thus only due to Cav3.2 channels. We showed that Cav3.2 channels were maintained in sperm by Western-blot and immunohistochernistry experiments. Calcium imaging experiments revealed that calcium influx in response to KCI was reduced in Cav3.2 null sperm in comparison to control cells, demonstrating that Cav3.2 channels were functional. On the other hand, no difference was noticed in calcium signaling induced by zona pellucida. Moreover, neither biochemical nor functional experiments, suggested the presence of Cav3.1 channels in sperm. Despite the Cav3.2 channels contribution in KCI-induced calcium influx, the reproduction parameters remained intact in Ca-v,3.2 deficient mice. These data demonstrate that in sperm, besides Cav3.2 channels, other types of VDCC are activated during the voltage-dependent calcium influx of AIR, these channels likely belonging to highvoltage activated Ca2+ channels family. The conclusion is that voltage-dependent calcium influx during AIR is due to the opening of redundant families of calcium channels.