1985
DOI: 10.1016/0014-5793(85)80835-8
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Pertussis toxin selectively abolishes hormone induced lowering of cytosolic calcium in GH3 cells

Abstract: Pertussis toxin, PT, abolishes inhibitory regulation of adenylate cyclase by cell surface receptors. Inhibitors of adenylate cyclase in GH, cells, namely somatostatin and the muscarinic cholinergic agonist carbachol, lower the cytosolic free Ca2+ concentration.[Ca2+], and cause hyperpolarization. These responses are selectively abolished by PT. It is concluded that the effects of somatostatin and carbachol to lower [Ca'+]i and to hyperpolarize are secondary to their inhibitory action on adenylate cyclase. In c… Show more

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Cited by 56 publications
(12 citation statements)
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“…This effect was less marked, however, than the decrease following cell treatment with all three hormones together (not shown). As reported previously for the parent cell line GH, (32), VIP stimulation of a population of control GH,C, cells led to a small transient rise in the average [Ca' 'Ii. dependent on extracellular C a 2 + .…”
Section: Hormone Treartnent Decreases a C Activitysupporting
confidence: 78%
“…This effect was less marked, however, than the decrease following cell treatment with all three hormones together (not shown). As reported previously for the parent cell line GH, (32), VIP stimulation of a population of control GH,C, cells led to a small transient rise in the average [Ca' 'Ii. dependent on extracellular C a 2 + .…”
Section: Hormone Treartnent Decreases a C Activitysupporting
confidence: 78%
“…Thorner, Hackett, Murad & MacLeod, 1980; Ray & Wallis, 1982¿>; Merritt & Brown, 1984). Studies employing the calcium indicators Quin-2 and Fura-2 (Schofield, 1983;Koch et al 1985;Schlegel, Wuarin, Zbaren et al 1985;Hart, Ray & Wallis, 1986;Malgaroli, Vallar, Elahi et al 1987) and 45Ca2+ (Schofield & Bicknell, 1978;Schrey, Clark & Franks, 1986) have confirmed this idea. Whether this effect is associated with changes in the intracellular concentration of inositol trisphosphate is not clear and is the subject of some controversy (Brown, Baird, Quilliam et al 1985;Canónico, Jarvis, Judd & MacLeod, 1986;Enjalbert, Sladeczek, Guillon et al 1986;Journot, Hornberger, Pantaloni et al 1987).…”
Section: Introductionmentioning
confidence: 92%
“…Several lines of evidence implicate G ␣i in signaling by the SSTRs. With the exception of modulation of the Na ϩ /H ϩ antiporter (20), the effector-modulating activities of the SSTRs are sensitive to pertussis toxin-catalyzed ADP ribosylation, which inactivates G ␣i and G ␣o (27,45,57). Antibodies directed at the carboxy-terminal domains of G ␣i1-3 block formation of high-affinity binding sites in soluble brain SSTRs, in agreement with inhibition of the formation of an SSTR-G ␣i complex (35).…”
mentioning
confidence: 98%