Estrogen suppresses melatonin-enhanced hyperactivation of hamster spermatozoa

• Published in: Journal of Reproduction and Development Vol. 61; no. 4; pp. 287 - 295
• Main Authors: FUJINOKI, Masakatsu, TAKEI, Gen L.
• Format: Journal Article
• Language: English
• Published: Japan THE SOCIETY FOR REPRODUCTION AND DEVELOPMENT 2015; The Society for Reproduction and Development
• Subjects: Animals; Estradiol; Estradiol - chemistry; Estradiol - metabolism; Estrogen Antagonists; Female; gamma-Aminobutyric Acid - metabolism; Hyperactivation; Kinetics; Male; Melatonin; Melatonin - agonists; Melatonin - antagonists & inhibitors; Melatonin - metabolism; Mesocricetus; Models, Biological; Non-genomic regulation; Original; Sperm Capacitation - drug effects; Sperm Motility - drug effects; Spermatozoa; Spermatozoa - cytology; Spermatozoa - drug effects; Spermatozoa - metabolism; Tamoxifen - pharmacology
• ISSN: 0916-8818; 1348-4400
• DOI: 10.1262/jrd.2014-116

Hamster sperm hyperactivation is enhanced by progesterone, and this progesterone-enhanced hyperactivation is suppressed by 17β-estradiol (17βE2) and γ-aminobutyric acid (GABA). Although it has been indicated that melatonin also enhances hyperactivation, it is unknown whether melatonin-enhanced hyperactivation is also suppressed by 17βE2 and GABA. In the present study, melatonin-enhanced hyperactivation was significantly suppressed by 17βE2 but not by GABA. Moreover, suppression of melatonin-enhanced hyperactivation by 17βE2 occurred through non-genomic regulation via the estrogen receptor (ER). These results suggest that enhancement of hyperactivation is regulated by melatonin and 17βE2 through non-genomic regulation.