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Title: Somatostatin-induced control of cytosolic free calcium in pituitary tumour cells
Authors: Petrucci, Cristina
Cervia, Davide
Buzzi, Marco
Biondi, Carla
Bagnoli, Paola
Keywords: Sst2 receptor;Agonists;Antagonist;Intracellular Ca2+;Cyclic AMP-dependent pathways;Cell culture;Fluorimetry;Confocal immunofluorescence
Issue Date: 2000
Publisher: Nature Publishing Group
Source: Petrucci, C. et al. 2000. Somatostatin-induced control of cytosolic free calcium in pituitary tumour cells. "British Journal of Pharmacology" 129(3): 471-484
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.
L'articolo è disponibile sul sito del nuovo editore
ISSN: 0007-1188
DOI: 10.1038/sj.bjp.0703075
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