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首页> 外文期刊>Life sciences >Rapid signaling responses in Sertoli cell membranes induced by follicle stimulating hormone and testosterone: calcium inflow and electrophysiological changes.
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Rapid signaling responses in Sertoli cell membranes induced by follicle stimulating hormone and testosterone: calcium inflow and electrophysiological changes.

机译：卵泡刺激素和睾丸激素诱导的Sertoli细胞膜快速信号响应：钙流入和电生理变化。

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This minireview describes the rapid signaling actions of follicle stimulating hormone (FSH) and testosterone in immature Sertoli cells mainly related to Ca(2+) inflow and the electrophysiological changes produced by hormones. The rapid membrane actions of FSH occur in a time frame of seconds to minutes, which include membrane depolarization and the stimulation of (45)Ca(2+) uptake. These effects can be prevented by pertussis toxin (PTX), suggesting that they are likely mediated by Gi-protein coupled receptor activation. Furthermore, these effects were inhibited by verapamil, a blocker of the L-type voltage-dependent Ca(2+) channel (VDCC). Finally, FSH stimulation of (45)Ca(2+) uptake was inhibited by the (phosphoinositide 3-kinase) PI3K inhibitor wortmannin. These results suggest that the rapid action of FSH on L-type Ca(2+) channel activity in Sertoli cells from pre-pubertal rats is mediated by the Gi/Gbetagamma/PI3Kgamma pathway, independent of its effects on insulin-like growth factor type I (IGF-I). Testosterone depolarizes the membrane potential and increases the resistance and the (45)Ca(2+) uptake in Sertoli cells of the seminiferous tubules of immature rats. These actions were nullified by diazoxide (K(+)(ATP) channel opener). Testosterone actions were blocked by both PTX and the phospholipase C (PLC) inhibitor U73122, suggesting the involvement of PLC - phosphatidylinositol 4-5 bisphosphate (PIP2) hydrolysis via the Gq protein in the testosterone-mediated pathway. These results indicate that testosterone acts on the Sertoli cell membrane through the K(+)(ATP) channels and PLC-PIP2 hydrolysis, which closes the channel, depolarizes the membrane and stimulates (45)Ca(2+) uptake. These results demonstrate the existence of rapid non-classical pathways in immature Sertoli cells regulated by FSH and testosterone.
机译：这份小型复习描述了主要与Ca（2+）流入和激素产生的电生理变化有关的未成熟Sertoli细胞中的卵泡刺激素（FSH）和睾丸激素的快速信号传导作用。 FSH的快速膜作用发生在几秒到几分钟的时间范围内，其中包括膜去极化和刺激（45）Ca（2+）吸收。这些作用可以通过百日咳毒素（PTX）来预防，表明它们可能是由Gi蛋白偶联受体激活介导的。此外，这些作用被维拉帕米抑制，维拉帕米是L型电压依赖性Ca（2+）通道（VDCC）的阻滞剂。最后，（磷酸肌醇3-激酶）PI3K抑制剂渥曼青霉素抑制了（45）Ca（2+）吸收的FSH刺激。这些结果表明，FSH对青春期前Sertoli细胞中L型Ca（2+）通道活性的快速作用是由Gi / Gbetagamma / PI3Kgamma途径介导的，而与它对胰岛素样生长因子类型的影响无关我（IGF-I）。睾丸激素使膜电位去极化并增加未成熟大鼠的生精小管的支持细胞中的抵抗力和（45）Ca（2+）摄取。通过重氮（K（+）（ATP）通道开放剂）使这些作用无效。 PTX和磷脂酶C（PLC）抑制剂U73122均阻断了睾丸激素的作用，这表明PLC-磷脂酰肌醇4-5双磷酸（PIP2）通过Gq蛋白水解参与了睾丸激素介导的途径。这些结果表明，睾丸激素通过K（+）（ATP）通道和PLC-PIP2水解作用作用于Sertoli细胞膜，关闭通道，使膜去极化并刺激（45）Ca（2+）吸收。这些结果证明了受FSH和睾丸激素调节的未成熟Sertoli细胞中存在快速的非经典途径。

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