Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-7-2
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0021-9541
pubmed:author
pubmed:issnType
Print
pubmed:volume
212
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
753-63
pubmed:meshHeading
pubmed-meshheading:17450521-Acrosome Reaction, pubmed-meshheading:17450521-Animals, pubmed-meshheading:17450521-Calcium Channels, T-Type, pubmed-meshheading:17450521-Calcium Signaling, pubmed-meshheading:17450521-Cells, Cultured, pubmed-meshheading:17450521-Female, pubmed-meshheading:17450521-Genotype, pubmed-meshheading:17450521-Litter Size, pubmed-meshheading:17450521-Male, pubmed-meshheading:17450521-Membrane Potentials, pubmed-meshheading:17450521-Mice, pubmed-meshheading:17450521-Mice, Inbred C57BL, pubmed-meshheading:17450521-Mice, Knockout, pubmed-meshheading:17450521-Phenotype, pubmed-meshheading:17450521-Potassium, pubmed-meshheading:17450521-Sperm Motility, pubmed-meshheading:17450521-Spermatozoa, pubmed-meshheading:17450521-Time Factors, pubmed-meshheading:17450521-Transfection
pubmed:year
2007
pubmed:articleTitle
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.
pubmed:affiliation
INSERM U836 Equipe 3, Laboratoire Canaux Calciques Fonctions et Pathologies, CEA/Grenoble, iRTSV, Université Joseph Fourier, Grenoble, France.
pubmed:publicationType
Journal Article, Comparative Study