Department of Zoology and Hawaii Institute of Marine Biology, University of Hawaii, Honolulu, HI, 96822, U.S.A..
Fish Physiol Biochem. 1989 Jun;7(1-6):11-9. doi: 10.1007/BF00004685.
The tilapia prolactin (PRL) cell responds rapidly (10-20 min) to small physiological changes in medium osmotic pressure (OP), releasing increasing quantities of hormone as medium OP is reduced. This release is rapidly (≤ 10 min) inhibited by somatostatin (SRIF). There is now extensive evidence that tilapia PRL cell function is regulated through the second messengers Ca(++) and cAMP. Our studies have shown that PRL release is augmented by treatments that lead to increased levels of intracellular Ca(++) or cAMP. On the other hand, PRL release is blocked when tissues are incubated in Ca(++)-depleted medium or upon the addition of Co(++), an inhibitor of Ca(++)-mediated processes. The use of(45)Ca(++) to characterize the movement of Ca(++) into PRL cells has provided evidence that an increase in the influx of extracellular Ca(++) may participate in PRL release upon exposure to hyposmotic medium. Our studies have also shown that SRIF suppresses the increase in(45)Ca(++) accumulation that is brought about when OP is reduced. We have also examined the effects of OP and SRIF on cAMP levels. The reduction of medium OP did not alter cAMP metabolism during 20 min of incubation. By contrast, cAMP accumulation in the presence of IBMX was enhanced at 1 hr of incubation in reduced OP. Thus, an increase in cAMP turnover may play a role in maintaining PRL release under sustained stimulation. SRIF reduced the accumulation of cAMP during 10 min of incubation with IBMX and also reduced the forskolin-stimulated increase in cAMP. Thus, SRIF may suppress adenylate cyclase activity. Finally, our studies have revealed that the forskolin-stimulated increase in cAMP levels is not dependent upon medium Ca(++). The presence of Ca(++) in the medium is required, however, for PRL release even when the cAMP messenger system has been activated. Moreover, cAMP accumulation was augmented when intracellular Ca(++) was increased. This raises the possibility that reduced OP may stimulate an increase in cAMP turnover indirectly through its action(s) on cytosolic Ca(++).
罗非鱼促乳素(PRL)细胞对培养基渗透压(OP)的微小生理变化反应迅速(10-20 分钟),随着培养基 OP 的降低,激素的分泌量逐渐增加。这种释放很快(≤10 分钟)被生长抑素(SRIF)抑制。现在有大量证据表明,罗非鱼 PRL 细胞的功能是通过第二信使 Ca(++)和 cAMP 调节的。我们的研究表明,通过增加细胞内 Ca(++)或 cAMP 水平的处理可以增强 PRL 的释放。另一方面,当组织在 Ca(++)耗尽的培养基中孵育或添加 Co(++)(一种抑制 Ca(++)介导过程的抑制剂)时,PRL 的释放会被阻断。使用(45)Ca(++)来描述 Ca(++)进入 PRL 细胞的运动,为渗透压降低时,细胞外 Ca(++)流入的增加可能参与 PRL 的释放提供了证据。我们的研究还表明,SRIF 抑制了渗透压降低时(45)Ca(++)积累的增加。我们还研究了 OP 和 SRIF 对 cAMP 水平的影响。在孵育 20 分钟期间,培养基 OP 的降低不会改变 cAMP 代谢。相比之下,在低 OP 存在 IBMX 的情况下,cAMP 积累在孵育 1 小时时增加。因此,cAMP 周转率的增加可能在持续刺激下维持 PRL 释放中发挥作用。SRIF 在与 IBMX 孵育 10 分钟时减少了 cAMP 的积累,也减少了 forskolin 刺激的 cAMP 增加。因此,SRIF 可能抑制腺苷酸环化酶的活性。最后,我们的研究表明,forskolin 刺激的 cAMP 水平增加不依赖于培养基中的 Ca(++)。然而,即使 cAMP 信使系统已被激活,培养基中 Ca(++)的存在也是 PRL 释放所必需的。此外,当细胞内 Ca(++)增加时,cAMP 积累增加。这提出了一种可能性,即低 OP 可能通过其对细胞质 Ca(++)的作用间接刺激 cAMP 周转率的增加。