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

Abstract

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.

Flagellar hyperactivation of bull and boar spermatozoa

“…In mouse and hamster epididymal spermatozoa, hyperactivation can be induced highly in vitro by incubation in a capacitation‐supporting medium, including HCO 3 − , Ca 2+ , and cholesterol acceptors . Researches with hamster epididymal spermatozoa proposed that occurrence of hyperactivation is hastened or delayed by the interaction with specific fluid components of female reproductive tracts, such as progesterone, 17β‐estradiol, melatonin, serotonin and γ‐aminobutyric acid, probably in order to modulate the timing of arrival of capacitated/acrosome‐reacted spermatozoa at the oviductal ampulla where ovulated oocytes are ready for the fertilization . In bull and boar ejaculated spermatozoa, by contrast, it may be difficult to induce hyperactivation highly by the simple incubation in the capacitation‐supporting medium .…”

“…[38][39][40][41] Researches with hamster epididymal spermatozoa proposed that occurrence of hyperactivation is hastened or delayed by the interaction with specific fluid components of female reproductive tracts, such as progesterone, 17β-estradiol, melatonin, serotonin and γaminobutyric acid, probably in order to modulate the timing of arrival of capacitated/acrosome-reacted spermatozoa at the oviductal ampulla where ovulated oocytes are ready for the fertilization. 42,43 In bull and boar ejaculated spermatozoa, by contrast, it may be difficult to induce hyperactivation highly by the simple incubation in the capacitation-supporting medium. [44][45][46][47] This suggests existence of strong suppressors (eg a calyculin-sensitive protein phosphatase) for hyperactivation in the spermatozoa from livestock.…”

Regulation of the bovine oviductal fluid proteome

“…PEBP1 has been identified among potential 'decapacitation factors' that were able, when added in vitro to suspensions of mouse spermatozoa, to inhibit sperm ability to undergo P 4 -induced acrosome reaction and to bind to the zona pellucida (Gibbons et al 2005, Nixon et al 2006. Thus, the increase in P 4 in the oviduct at the time of ovulation, in addition to triggering sperm hyperactivation (Fujinoki et al 2016), may allow the inhibition of such decapacitation factor and finally contribute to the presence of spermatozoa able to fertilize around the oocyte.…”

Effect of Lepidium meyenii on in vitro fertilization via improvement in acrosome reaction and motility of mouse and human sperm

“…It is possible that Maca induces the acrosome reaction and hyperactivation because of an increase in cAMP and the number of spermatozoa with high MMP. Furthermore, it has recently been suggested that some hormones, including progesterone, melatonin, and serotonin, enhance hyperactivation through specific membrane receptors and that 17β‐estradiol suppresses such enhancement by progesterone and melatonin via a membrane estrogen receptor . Because plant extracts can have several functions, including estrogenic actions, depending on the flavonoids present, it is possible that Maca also has a specific estrogenic action.…”