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  • Title: Involvement of the cAMP messenger system and extracellular Ca(2+) during hyposmotically-induced prolactin release in the Mozambique tilapia.
    Author: Seale AP, Mita M, Hirano T, Gordon Grau E.
    Journal: Gen Comp Endocrinol; 2011 Jan 15; 170(2):401-7. PubMed ID: 21050855.
    Abstract:
    In accord with its role in freshwater osmoregulation, prolactin (PRL) release from the tilapia pituitary is stimulated by small, physiologically relevant reductions in plasma osmolality, a response that is mediated by an acute influx of intracellular Ca(2+) through stretch-activated Ca(2+)channels. In the present study, the role of the calcium and cyclic AMP (cAMP) messenger system in the transduction of a response to a hyposmotic stimulus was examined using dispersed PRL cells and PRL cell membrane preparations from freshwater-acclimated tilapia. When PRL cells were treated with the phosphodiesterase (PDE) inhibitor, 3-isobutyl-1-methylxanthine (IBMX) (100μM), significant increases in cAMP levels and PRL release were observed at 1h. Exposure to reduced medium osmolality (300 mOsmolal) in the presence of IBMX further augmented PRL release. Depletion of Ca(2+) from the incubation medium blocked PRL release even in the presence of IBMX. By contrast, exposure of PRL cells to cholera toxin (CTX), an activator of adenylyl cyclase (AC), stimulated PRL release and cAMP accumulation in both the presence and absence of extracellular Ca(2+). On the other hand, treatment with the Ca(2+) ionophore A23187, which elicits a large rise in intracellular free Ca(2+), reduced cAMP accumulation. Likewise, the AC activity of a PRL cell membrane preparation was reduced as extracellular Ca(2+) concentration increased from 0.1 to 1 μM. These results indicate that: (1) the stimulation of PRL release and cAMP formation by a fall in extracellular osmolality are Ca(2+)-dependent; (2) large increases in intracellular Ca(2+) attenuate cAMP formation; (3) direct agonists of cAMP messenger system, such as cholera toxin, however, stimulate PRL release independently of the extracellular Ca(2+). These findings add to the evidence that the osmosensitive response of the tilapia PRL cell is mediated through a Ca(2+)-dependent mechanism. Nevertheless, the present findings also suggest that tilapia PRL cells have the ability to rapidly augment release PRL both via a Ca(2+)-dependent manner and via a cAMP-dependent pathway in the absence of extracellular Ca(2+).
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