The tilapia prolactin cell: A model for stimulus-secretion coupling

Abstract

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(++).