The mechanisms of cholinergic stimulation of gastrin cells were studied in the rat pancreatic cell line B6 RIN. Carbachol induced an increase in intracellular Ca2+ and stimulated gastrin release in a dose-dependent manner over the range 10−5-10−3 M. These effects were completely abolished by atropine, suggesting the implication of muscarinic cholinergic receptors. The binding properties of these receptors were investigated. [N-Methyl-3H]scopolamine ([3h]nms) binding on cell homogenates was time-dependent, saturable and consistent with a single high-affinity binding class (K d = 39.5 pM, and B max = 7.9 81229-H/asset/equation/feb2001457939081229h-math-si1.gif?v=1&s=e348f19e4531b9da80734d892f8b8f2d15f13a9b)
DNA). Carbachol competitively inhibited [3H]NMS binding. The potency of inhibition of [3H]NMS binding by subtype selective antagonists was hexahydrodifenidol > pirenzepine > AF-DX 116. These results suggest the M3, muscarinic receptors may be involved in the carbachol-induced gastrin release from B6 RIN cells.
