EUREKALERT, UNIVERSITY OF MONTREAL AND MAISONNEUVE-ROSEMONT HOSPITAL RESEARCH CENTERThe many barriers to the development of male contraception include potential effects on sex drive, irreversibility, and the sheer magnitude of sperm production—the human testes produce around 1,000 sperm every minute. Now, Australian researchers have shown that male mice lacking both the P2X1-purinoceptor and α1A-adrenoceptor are infertile, but behave normally and can father offspring by in vitro fertilization. Their work was published in Proceedings of the National Academy of Sciences this week (December 2).
Both the P2X1-purinoceptor, which is a ligand-gated ion channel, and α1A-adrenoceptor, which is a G protein-coupled receptor, are activated to cause contractions of the smooth muscle that lines the vas deferens, which in turn causes sperm to be pumped out during ejaculation. The researchers generated double knockout mice for P2X1-purinoceptor and α1A-adrenoceptor. While these male mice engaged in normal sexual behavior, they did not father offspring. The scientists demonstrated that the contractility of the vas deferens was severely compromised in the double knockout mice, but their sperm could be used to fertilize eggs in vitro, leading to live offspring. The findings suggested that if infertility could be induced by pharmacological inhibition of these receptors, it might be reversible.
“The sperm stay in the storage site ...
