Chronic Exposure to Pertussis Toxin Alters Muscarinic Receptor‐Mediated Regulation of Cyclic AMP Metabolism in Neuroblastoma × Glioma NG108–15 Hybrid Cells

Abstract

Chronic pertussis toxin treatment (5 days) of NG108-15 neuroblastoma X glioma hybrid cells had no significant effect on basal cyclic AMP levels whereas it effectively blocked the inhibitory action of acute (10 min) exposure of carbachol (10(-4)M) on intracellular cyclic AMP accumulation, stimulated by prostaglandin E1. This action of pertussis toxin was found to be long lasting: exposure of the cells to pertussis toxin (100 ng/ml) for only 24 h followed by a 5-day withdrawal period still was shown effective on day 7 in abolishing the inhibitory action of carbachol on prostaglandin E1-stimulated cyclic AMP production. Chronic exposure (5 days) of NG108-15 cells to carbachol (10(-5)M) causes an increase in basal cyclic AMP levels by 98%, and a desensitization of the muscarinic inhibition of cyclic AMP accumulation, assessed after a 24-h withdrawal period. When carbachol treatment is carried out in the presence of pertussis toxin (100 ng/ml) both of these effects of carbachol are abolished.

Chronic Opioid Treatment Induces Adenylyl Cyclase V Superactivation

“…The superactivation phenomenon has previously been shown in NG 108-15 cells when inhibitory ␦-opioid and muscarinic receptors were exposed to chronic treatment with agonists of these receptors (Hamprecht, 1977;Sharma et al, 1975;Westlind-Danielsson et al, 1988). In Fig.…”

Muscarinic potentiation of excitatory amino acid‐evoked dopamine release in mesencephalic cells: Specificity for the NMDA response and role of intracellular messengers

“…In experiments with staurosporine, H8 and W7, these drugs were present 20 min before, as well as during, the basal and stimulated release periods. In experiments with pertussis toxin, cultures were incubated with pertussis toxin (500 ng/ml) for 19 h and the toxin was removed prior to loading the cells with 13HlDA and measuring I3H1DA release; previous studies have demonstrated that this concentration of the toxin is sufficient to effectively inhibit G protein mediated functions and to ADP ribosylate membrane-associated G proteins in a variety of cell culture preparations derived from the nervous system (Westlind-Danielsson et al, 1988;Woods et al, 1989;Luini and De Matteis, 1990;Ohara-Imaizumi et al, 1992;Prezeau et al, 1992). Radioactivity in aliquots of release media aspirated from the cells was quantitated using liquid scintillation spectrometry.…”