Non-genomic regulation and disruption of spermatozoal in vitro hyperactivation by oviductal hormones

The Journal of Physiological Sciences - Tập 66 - Trang 207-212 - 2015
Masakatsu Fujinoki1, Gen L. Takei1, Hiroe Kon2
1Department of Physiology, School of Medicine, Dokkyo Medical University, Mibu, Japan
2Laboratory Animal Research Center, School of Medicine, Dokkyo Medical University, Mibu, Japan

Tóm tắt

During capacitation, motility of mammalian spermatozoon is changed from a state of “activation” to “hyperactivation.” Recently, it has been suggested that some hormones present in the oviduct are involved in the regulation of this hyperactivation in vitro. Progesterone, melatonin, and serotonin enhance hyperactivation through specific membrane receptors, and 17β-estradiol suppresses this enhancement by progesterone and melatonin via a membrane estrogen receptor. Moreover, γ-aminobutyric acid suppresses progesterone-enhanced hyperactivation through the γ-aminobutyric acid receptor. These hormones dose-dependently affect hyperactivation. Although the complete signaling pathway is not clear, progesterone activates phospholipase C and protein kinases and enhances tyrosine phosphorylation. Moreover, tyrosine phosphorylation is suppressed by 17β-estradiol. This regulation of spermatozoal hyperactivation by steroids is also disrupted by diethylstilbestrol. The in vitro experiments reviewed here suggest that mammalian spermatozoa are able to respond to effects of oviductal hormones. We therefore assume that the enhancement of spermatozoal hyperactivation is also regulated by oviductal hormones in vivo.

Tài liệu tham khảo

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