Key result
CaV3.2 primarily mediates T-type calcium currents in mouse spermatogenic cells with negligible CaV3.1 contribution.
Why the study?
The molecular characterization of the T-type calcium channel in spermatogenic cells remains debated, with unclear contributions of CaV3.1 and CaV3.2 subunits.
The study demonstrates that Ca(V)3.2, rather than Ca(V)3.1, is the primary functional T-type calcium channel in mammalian spermatogenic cells.
No immediate clinical implications; leaves open CaV3.2 targeting in human male fertility research.
Mammalian acrosome reaction (AR) requires successive activation of three different types of calcium channels (T-type channels, Inositol-3-phosphate (InsP3) receptors, and TRPC2 channels). All the calcium signaling is under the control of the activation of the first-one, a T-type calcium channel. The molecular characterization of the T-type calcium channel is still a matter of debate, previous reports showing the presence of transcripts for Ca(V)3.1 and Ca(V)3.2 subunits. Using mice deficient for Ca(V)3.1 subunit, we show that the T-type current density in spermatogenic cells is not reduced in deficient mice versus control mice. We characterized the biophysical and pharmacological properties of T-type current in spermatogenic cells from Ca(V)3.1 deficient mice. Biophysical and pharmacological properties of spermatogenic T-type current from wild-type and Ca(V)3.1 deficient mice demonstrate that Ca(V)3.3 does not contribute to T-type current. Moreover, nickel and amiloride inhibit T-type currents in deficient and wild-type mice with similar potencies. These results demonstrate that T-type currents in spermatogenic cells is due to Ca(V)3.2 subunit and that Ca(V)3.1 contributes to a very negligible extent to the T-type currents. Thus, the deficient Ca(V)3.1 mouse model allows the characterization of native Ca(V)3.2 currents in spermatogenic cells. Spermatogenic Ca(V)3.2 currents present specific feature in comparison to the cloned Ca(V)3.2 current so far. More particularly, the time-dependence of recovery from short-term inactivation of native spermatogenic Ca(V)3.2 is close to 100 millisecond, a value expected for Ca(V)3.1 current.
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Stamboulian et al. (2003) studied this question. CaV3.1 deficiency vs. Wild-type mice was evaluated on T-type current density and biophysical/pharmacological properties. T-type calcium currents in mouse spermatogenic cells are primarily mediated by the CaV3.2 subunit, with CaV3.1 contributing to a negligible extent.
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