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促性腺激素释放激素诱导的大鼠促性腺激素细胞钙振荡刺激的节律性胞吐作用。

Rhythmic exocytosis stimulated by GnRH-induced calcium oscillations in rat gonadotropes.

作者信息

Tse A, Tse F W, Almers W, Hille B

机构信息

Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle 98195.

出版信息

Science. 1993 Apr 2;260(5104):82-4. doi: 10.1126/science.8385366.

Abstract

In pituitary gonadotropes, gonadotropin-releasing hormone (GnRH) induces the rhythmic release of Ca2+ from an inositol 1,4,5-trisphosphate (IP3)-sensitive store. Simultaneous measurement of the concentration of cytosolic free Ca2+ ([Ca2+]i) and exocytosis in single identified gonadotropes showed that each elevation of [Ca2+]i induced a burst of exocytosis. These phenomena were largely suppressed by buffering of [Ca2+]i but persisted in the absence of extracellular Ca2+. Activation of voltage-gated Ca2+ channels by brief depolarizations seldom supplied enough Ca2+ for exocytosis, but [Ca2+]i elevations induced by photolysis of caged IP3 did trigger exocytosis, confirming that GnRH-stimulated gonadotropic hormone secretion is closely coupled to intracellular Ca2+ release. Agonist-induced oscillations of [Ca2+]i in secretory cells may be a mechanism to optimize the secretory output while avoiding the toxic effects of sustained elevation of [Ca2+]i.

摘要

在垂体促性腺细胞中,促性腺激素释放激素(GnRH)诱导从对肌醇1,4,5 -三磷酸(IP3)敏感的储存库中呈节律性释放Ca2+。在单个已鉴定的促性腺细胞中同时测量胞质游离Ca2+浓度([Ca2+]i)和胞吐作用,结果显示[Ca2+]i的每次升高都会引发一阵胞吐作用。这些现象在很大程度上因[Ca2+]i的缓冲而受到抑制,但在无细胞外Ca2+的情况下仍会持续。短暂去极化对电压门控Ca2+通道的激活很少能为胞吐作用提供足够的Ca2+,但通过光解笼化IP3诱导的[Ca2+]i升高确实能触发胞吐作用,这证实了GnRH刺激的促性腺激素分泌与细胞内Ca2+释放密切相关。激动剂诱导的分泌细胞中[Ca2+]i振荡可能是一种优化分泌输出的机制,同时避免[Ca2+]i持续升高的毒性作用。

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