{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T20:40:04Z","timestamp":1790541604414,"version":"4.1.0"},"reference-count":38,"publisher":"The Endocrine Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,3,1]]},"abstract":"<jats:p>Our previous study demonstrated that FSH-induced immediate Ca2+ influx in rat Sertoli cells (SCs) is mediated by the G\u03b1h\/phospholipase C-\u03b41 (PLC-\u03b41) signaling pathway. As to which Ca2+ channel is responsible for such Ca2+ influx was not understood. In this study, thapsigargin triggered an in-store calcium release and evoked a 1.5-fold elevation of intracellular Ca2+ in Ca2+-free media, whereas FSH exhibited no effect. The readdition of CaCl2 (2.5 mm) to FSH-pretreated or thapsigargin-sensitized SCs in Ca2+-free media immediately elicited a rapid Ca2+ influx or a 2-fold increase of second intracellular Ca2+ elevation, respectively. The addition of Ca2+ chelator EGTA (0.2 mm) reduced the FSH-induced elevation of intracellular Ca2+ in SCs incubated with CaCl2. However, pretreatment with dantrolene (25 \u03bcM), which inhibits in-store calcium release, did not affect the FSH-induced elevation of intracellular Ca2+. NiCl2 (10 \u03bcM), a T-type calcium channel blocker, abolished the FSH-induced SC Ca2+ influx. Furthermore, mibefradil (10 and 100 \u03bcm), another specific blocker for T-type Ca2+ channels, dose-dependently suppressed the FSH-induced Ca2+ influx. In contrast, nifedipine (10 and 50 \u03bcm) or \u03c9-conotoxin GVIA (100 and 500 nm), blocker of L- or N-type Ca2+ channels, respectively, did not affect the FSH-induced SC Ca2+ influx. On the other hand, FSH-induced Ca2+ influx was significantly reduced by pretreatment of SCs with myristoylated synthetic peptide (0.1 and 1 \u03bcm) of PLC-\u03b41 fragment TIPWNSLKQGYRHVHLL but not affected by 2\u2032,5\u2032-dideoxyadenosine (3 and 15 \u03bcm), a selective inhibitor of adenylate cyclase. In conclusion, the FSH-induced G\u03b1h\/PLC-\u03b41 pathway-dependent Ca2+ influx of rat SCs is mediated by T-type Ca2+ channels and independent of in-store calcium release.<\/jats:p>","DOI":"10.1210\/en.2007-1244","type":"journal-article","created":{"date-parts":[[2007,12,7]],"date-time":"2007-12-07T01:39:52Z","timestamp":1196991592000},"page":"1031-1037","source":"Crossref","is-referenced-by-count":18,"title":["Follicle-Stimulating Hormone-Induced G\u03b1h\/Phospholipase C-\u03b41 Signaling Mediating a Noncapacitative Ca2+ Influx through T-Type Ca2+ Channels in Rat Sertoli Cells"],"prefix":"10.1210","volume":"149","author":[{"given":"Tsung-Hsuan","family":"Lai","sequence":"first","affiliation":[{"name":"Division of Reproduction Medicine (T.-H.L.), Department of Obstetrics and Gynecology, Cathay General Hospital, Taipei, Taiwan 106, Republic of China"},{"name":"Fu Jen Catholic University School of Medicine (T.-H.L.), Taipei, Taiwan, 242, Republic of 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