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Multiple Transduction Mechanisms Activated by the Neuropeptide Somatostatin

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Receptor-Receptor Interactions

Part of the book series: Wenner-Gren Center International Symposium Series ((WGS))

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Abstract

Because somatostatin inhibits secretion in a wide variety of target cells, studies probing its mechanism of action have focused on the role played by two of the intracellular messengers known to regulate secretory processes: cyclic AMP and calcium (see reviews 1–5). Thus, somatostatin has been proposed to both regulate the concentrations of these intracellular messengers and also to modify their effectiveness. Although direct evidence showing that somatostatin is able to regulate the potency of either cyclic AMP or calcium is still lacking, recent studies have begun to clarify how somatostatin alters the concentrations of these two intracellular mediators and the extent to which such changes are involved in eliciting somatostatin’s effects on secretion. This review summarizes studies on the mechanisms by which somatostatin inhibits growth hormone (GH) and prolactin (PRL) secretion from the GH4C1 pituitary cell line. These cells have two major advantages for elucidating the biochemical mediators involved in somatostatin action. First, the effects of somatostatin to inhibit GH and PRL secretion in GH4C1 cells parallel its actions in estrogen primed pituitary cells both in primary culture and in vivo (4,6–9). Second, GH4C1 cells are clonal in origin and therefore both hormonal and biochemical responses are produced by the same population of target cells and can be quantitatively correlated.

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© 1987 The Wenner-Gren Center

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Schonbrunn, A. (1987). Multiple Transduction Mechanisms Activated by the Neuropeptide Somatostatin. In: Fuxe, K., Agnati, L.F. (eds) Receptor-Receptor Interactions. Wenner-Gren Center International Symposium Series. Palgrave Macmillan, London. https://doi.org/10.1007/978-1-349-08949-9_23

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