THE TILAPIA PROLACTIN CELL - A MODEL FOR STIMULUS-SECRETION COUPLING

THE TILAPIA PROLACTIN CELL - A MODEL FOR STIMULUS-SECRETION COUPLING
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DOI:
10.1007/bf00004685
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发表时间:
1989-06-01
影响因子:
2.9
通讯作者:
HELMS, LMH
HELMS, LMH
中科院分区:
农林科学3区
文献类型:
--
作者:
GRAU, EG;HELMS, LMH

文献摘要

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罗非鱼催乳素(PRL)细胞对中等渗透压(OP)中的小的生理变化快速响应(10-20分钟),随着中等OP降低释放增加量的激素。生长抑素(SRIF)可快速(≤ 10 min)抑制该释放。现在有大量的证据表明,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,PRL的释放增加的治疗,导致细胞内Ca++或cAMP的水平增加。另一方面,当组织在Ca++耗尽的培养基中孵育或加入Co++(Ca++介导过程的抑制剂)时,PRL释放被阻断。用~(45)Ca ~(++)来表征Ca ~(++)向PRL细胞内的运动,为低渗条件下细胞外Ca ~(++)内流的增加可能参与PRL的释放提供了证据。我们的研究还表明,SRIF抑制了OP降低时45 Ca ++蓄积的增加。我们还检查了OP和SRIF对cAMP水平的影响。在20分钟的孵育过程中,培养基OP的减少没有改变cAMP代谢。相比之下,cAMP的积累在IBMX的存在下,增加在1小时的孵育减少OP。因此,在cAMP营业额的增加可能发挥作用,在持续刺激下,保持PRL的释放。SRIF减少了cAMP的积累,在10分钟的孵育与IBMX,也减少了毛喉素刺激的cAMP的增加。因此,SRIF可能抑制腺苷酸环化酶活性。最后,我们的研究表明,毛喉素刺激的cAMP水平的增加是不依赖于介质Ca++。然而,即使cAMP信使系统被激活,介质中的Ca++的存在对于PRL的释放也是必需的。此外,当细胞内Ca++增加时,cAMP积累增加。这增加了OP减少可能通过其对细胞溶质Ca++的作用间接刺激cAMP周转增加的可能性。
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 of45Ca++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 in45Ca++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++.