title: 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 AR 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 AR and sperm motility, independently of pharmacological tools. The inward current was fully abolished in spermatogenic cells from Ca(V)3.2 deficient mice. This current is thus only due to Ca(V)3.2 channels. We showed that Ca(V)3.2 channels were maintained in sperm by Western-blot and immunohistochemistry experiments. Calcium imaging experiments revealed that calcium influx in response to KCl was reduced in Ca(V)3.2 null sperm in comparison to control cells, demonstrating that Ca(V)3.2 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 Ca(V)3.1 channels in sperm. Despite the Ca(V)3.2 channels contribution in KCl-induced calcium influx, the reproduction parameters remained intact in Ca(V)3.2 deficient mice. These data demonstrate that in sperm, besides Ca(V)3.2 channels, other types of VDCC are activated during the voltage-dependent calcium influx of AR, these channels likely belonging to high-voltage activated Ca(2+) channels family. The conclusion is that voltage-dependent calcium influx during AR is due to the opening of redundant families of calcium channels.
authors: INSERM U836 Equipe 3, Laboratoire Canaux Calciques Fonctions et Pathologies, CEA/Grenoble, iRTSV, Université Joseph Fourier, Grenoble, France.
authors: Jessica
authors: J
authors: Escoffier
authors: Sylvie
authors: S
authors: Boisseau
authors: Catherine
authors: C
authors: Serres
authors: Chien-Chang
authors: CC
authors: Chen
authors: Daesoo
authors: D
authors: Kim
authors: Séverine
authors: S
authors: Stamboulian
authors: Hee-Sup
authors: HS
authors: Shin
authors: Kevin P
authors: KP
authors: Campbell
authors: Michel
authors: M
authors: De Waard
authors: Christophe
authors: C
authors: Arnoult
mesh_terms: D020101:Acrosome Reaction; D000818:Animals; D020747:Calcium Channels, T-Type / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D020013:Calcium Signaling; D002478:Cells, Cultured; D005260:Female; D005838:Genotype; D008098:Litter Size; D008297:Male; D008564:Membrane Potentials; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D010641:Phenotype; D011188:Potassium / Q000378:metabolism; D013081:Sperm Motility; D013094:Spermatozoa / Q000378:metabolism*; D013997:Time Factors; D014162:Transfection
chemical_list: C498197:Cacna1g protein, mouse; C504883:Cacna1h protein, mouse; D020747:Calcium Channels, T-Type; D011188:Potassium