The DSpace digital repository system captures, stores, indexes, preserves, and distributes digital research material. http://http://dspace.unitus.it:80 2013-05-25T01:41:20Z 2013-05-25T01:41:20Z Petrucci, Cristina Cervia, Davide Buzzi, Marco Biondi, Carla Bagnoli, Paola http://hdl.handle.net/2067/1430 2011-07-18T14:34:42Z 1999-12-31T23:00:00Z

Title: Somatostatin-induced control of cytosolic free calcium in pituitary tumour cells Authors: Petrucci, Cristina; Cervia, Davide; Buzzi, Marco; Biondi, Carla; Bagnoli, Paola Abstract: 1 In rat pituitary tumor cells (GC cells), spontaneous oscillations of the intracellular concentration of Ca2+ ([Ca2+]i) induce growth hormone (GH) secretion that is inhibited by octreotide, a somatostatin (SRIF) agonist which binds to SRIF subtype (sst) receptor 2. The effects of its functional activation on the control of [Ca2+]i were investigated using fluorimetric measurements of [Ca2+]i. 2 SRIF decreases the basal [Ca2+]i and the [Ca2+]i rise in response to forskolin (FSK) through the inhibition of L-type voltage-dependent Ca2+ channels. 3 Pretreatment with octreotide or with L-Tyr8Cyanamid 154806, a sst2 receptor antagonist, abolishes the SRIF-induced inhibition of [Ca2+]i. Octreotide is known to operate through agonist-induced desensitization, while the antagonist operates through receptor blockade. 4 sst1 and sst2 receptor-immunoreactivities (-IRs) are localized to cell membranes. sst2, but not sst1 receptor-IR, internalizes after cell exposure to octreotide. 5 SRIF-induced inhibition of basal [Ca2+]i or FSK-induced Ca2+ entry is blocked by pertussis toxin (PTX). 6 FSK-induced cAMP accumulation is only partially decreased by SRIF or octreotide, indicating that sst2 receptors are coupled to intracellular pathways other than adenylyl cyclase (AC) inhibition. 7 In the presence of H-89, an inhibitor of cAMP-dependent protein kinase (PKA), SRIF-induced inhibition of basal [Ca2+]i is still present, although reduced in amplitude. 8 SRIF inhibits [Ca2+]i by activating sst2 receptors. Inhibition of AC activity is only partly responsible for this effect, and other transduction pathways may be involved. Description: L'articolo è disponibile sul sito del nuovo editore http://onlinelibrary.wiley.com/

1999-12-31T23:00:00Z Dal Monte, Massimo Petrucci, Cristina Vasilaki, Anna Cervia, Davide Grouselle, Dominique Epelbaum, Jacques Kreienkamp, Hans-Jurgen Richter, Dietmar Hoyer, Daniel Bagnoli, Paola http://hdl.handle.net/2067/1449 2011-06-28T10:54:54Z 2002-12-31T23:00:00Z

Title: Genetic deletion of somatostatin receptor 1 alters somatostatinergic transmission in the mouse retina Authors: Dal Monte, Massimo; Petrucci, Cristina; Vasilaki, Anna; Cervia, Davide; Grouselle, Dominique; Epelbaum, Jacques; Kreienkamp, Hans-Jurgen; Richter, Dietmar; Hoyer, Daniel; Bagnoli, Paola Abstract: In the mammalian retina, sparse amacrine cells contain somatostatin-14 (SRIF) which acts at multiple levels of neuronal circuitry through distinct SRIF receptors (sst1-5). Among them, the sst1 receptor has been localized to SRIF-containing amacrine cells in the rat and rabbit retina. Little is known about sst1 receptor localization and function in the mouse retina. We have addressed this question in the retina of mice with deletion of sst1 receptors (sst1 KO mice). In the retina of wild type (WT) mice, sst1 receptors are localized to SRIF-containing amacrine cells whereas in the retina of sst1 KO mice, sst1 receptors are absent. sst1 receptor loss causes a significant increase in retinal levels of SRIF whereas it does not affect SRIF messenger RNA indicating that sst1 receptors play a role in limiting retinal SRIF at the post-transcriptional level. As another consequence of sst1 receptor loss, levels of expression of sst2 receptors are significantly higher than in control retinas. Together, these findings provide the first demonstration of prominent compensatory regulation in the mouse retina as a consequence of a distinct SRIF receptor deletion. The fact that in the absence of the sst1 receptor, retinal SRIF increases in concomitance with an increase in sst2 receptors suggests that SRIF may regulate sst2 receptor expression and that this regulatory process is controlled upstream by the sst1 receptor. This finding can be important in the design of drugs affecting SRIF function, not only in the retina, but also elsewhere in the brain. Description: L'articolo è disponibile sul sito dell'editore http://www.sciencedirect.com/

2002-12-31T23:00:00Z Cervia, Davide Petrucci, Cristina Bluet-Pajot, Marie Thérèse Epelbaum, Jacques Bagnoli, Paola http://hdl.handle.net/2067/1441 2011-06-28T12:50:21Z 2001-12-31T23:00:00Z

Title: Inhibitory control of growth hormone secretion by somatostatin in rat pituitary GC cells: sst2 but not sst1 receptors are coupled to an inhibition of single-cell intracellular free calcium concentrations Authors: Cervia, Davide; Petrucci, Cristina; Bluet-Pajot, Marie Thérèse; Epelbaum, Jacques; Bagnoli, Paola Abstract: Rat pituitary tumor cells (GC cells) exhibit spontaneous oscillations of intracellular free calcium concentration ([Ca2+]i) that allow a continuous release of growth hormone (GH). Of the SRIH receptor subtypes (sst receptors) mediating SRIH action, sst1 and sst2 receptors are highly expressed by GC cell membranes. In the present study, the effects of sst1 or sst2 receptor activation on single-cell [Ca2+]i were investigated in GC cells by confocal fluorescence microscopy. In addition, the effects of sst1 or sst2 receptor activation on GH secretion were also studied. Our results demonstrate that SRIH decreases [Ca2+]i baseline and almost completely blocks Ca2+ transients through the activation of sst2 but not of sst1 receptors. In contrast, SRIH effectively inhibits GH secretion through the activation of both sst1 and sst2 receptors. Blocking Ca2+ transients is less efficient than SRIH to inhibit GH release. The cyclic octapeptide, CYN-154806, antagonizes sst2 receptors at [Ca2+]i since it abolishes the sst2 receptor-mediated inhibition of [Ca2+]i without affecting single-cell Ca2+ signals. Unexpectedly, CYN-154806 alone potently inhibits GH secretion through the involvement of pertussis toxin-sensitive G proteins. In conclusion, the present results demonstrate that SRIH inhibition of GH release in GC cells involves mechanisms either dependent or independent on SRIH modulation of [Ca2+]i. The implications of CYN-154806 inhibition of GH secretion are discussed. Description: L'articolo è disponibile sul sito dell'editore http://www.karger.com

2001-12-31T23:00:00Z