Although it is accepted that progesterone (P) induces acrosome reaction through non-genomic regulation, it is not well known if P also affects hyperactivation of sperm. Hamster spermatozoa were hyperactivated by incubation for 4 h on modified Tyrode's albumin lactate pyruvate medium and recorded on a DVD via a charge-coupled device camera attached to a microscope with phase-contrast illumination and a small CO incubator. Phosphorylation of proteins was detected by western blotting using antiphosphotyrosine antibodies. Sperm hyperactivation was significantly increased and accelerated by a non-genomic signal of P. Although acceleration of motility of hyperactivated sperm occurred with 10, 20 and 40 ng/mL P, the most effective concentration was 20 ng/mL. Progesterone also significantly increased 80-kDa tyrosine phosphorylation of sperm proteins. Both extracellular Ca and albumin were essential for sperm hyperactivation, and the former was also essential for maintaining sperm flagellar movement. Moreover, phospholipase C (PLC) was associated with the regulation of hyperactivation by P. It is likely that P regulates sperm hyperactivation by a non-genomic signal in relation to tyrosine phosphorylation and PLC. (Reprod Med Biol 2008;: 63-74).
The effects of melatonin on reproductive function were examined using hamster spermatozoa. When 1 pM to 1 mM melatonin was added to the mTALP medium, hyperactivation was significantly enhanced. Antagonists and agonists of the melatonin receptor (i.e., MT1 and MT2) were added to the medium. Luzindole, an MT1 and MT2 competitive antagonist, significantly inhibited melatonin-induced hyperactivation, whereas the MT2-specific antagonists, 4-phenyl-2-propionamidotetralin and N-pentanoyl-2-benzyltryptamine, had no effect. Moreover, hyperactivation was significantly enhanced when non-specific agonists, such as 6-chloromelatonin and 2-iodomelatonin, were added to the medium. 8-Methoxy-2-propionamidotetralin, which is a strong MT2 agonist and a weak MT1 agonist, significantly increased hyperactivation, although the effect was weak. Therefore, it is likely that melatonin enhances sperm hyperactivation via the MT1 receptor.
In this study, I examined whether sperm hyperactivation in hamster is regulated by steroid hormones such as estrogen (estradiol, E 2 ) and progesterone. Although sperm hyperactivation was enhanced by progesterone, 17b-estradiol (17bE 2 ) itself did not affect sperm hyperactivation. However, 17bE 2 suppressed progesterone-enhanced hyperactivation in a concentration-dependent manner through non-genomic pathways when spermatozoa were exposed to 17bE 2 at the same time or before exposure to progesterone. When spermatozoa were exposed to 17bE 2 after exposure to progesterone, 17bE 2 did not suppress progesterone-enhanced hyperactivation. Moreover, 17a-estradiol, an inactive isomer of E 2 , did not suppress progesterone-enhanced hyperactivation. Observations using a FITC-conjugated 17bE 2 showed that it binds to the acrosome region of the sperm head. Binding of 17bE 2 to spermatozoa was not inhibited by progesterone, although 17bE 2 did not suppress progesterone-enhanced hyperactivation when spermatozoa were exposed to 17bE 2 after exposure to progesterone. On the other hand, binding of progesterone to spermatozoa was also not inhibited by 17bE 2 even if progesterone-enhanced hyperactivation was suppressed by 17bE 2 . Although tyrosine phosphorylations of sperm proteins were enhanced by progesterone, enhancement of tyrosine phosphorylations by progesterone was suppressed by 17bE 2 . Moreover, tyrosine phosphorylations were inhibited by 17bE 2 when only 17bE 2 was added to the medium. From these results, it is likely that 17bE 2 competitively suppresses progesterone-enhanced hyperactivation through the inhibition of tyrosine phosphorylations via non-genomic pathways.
The effects of serotonin on reproductive function were examined using hamster spermatozoa. When serotonin at concentrations from 1 fmol/l to 1 mmol/l was added to modified Tyrode's albumin lactate pyruvate (mTALP) medium, hyperactivation was significantly enhanced. Agonists and antagonists of 5-hydroxytryptamine hydrochloride (5-HT) receptors (5-HT 2 and 5-HT 4 receptors) were added to the medium. Both 5-HT 2 and 5-HT 4 receptor agonists significantly enhanced hyperactivation, although the effect was greater than the former. However, both 5-HT 2 and 5-HT 4 receptor antagonists significantly suppressed serotonin-enhanced hyperactivation, with the former suppressing stimulation by a lower concentration of serotonin than the latter. These results indicate that serotonin enhances hyperactivation via 5-HT 2 and/or 5-HT 4 receptors in a dose-dependent manner.
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