Effect of neural stimulation on acinar cell membrane potentials in isolated pancreas and salivary gland segments.
The effect of cholinergic neural excitation by field stimulation on the acinar cell membrane potential was investigated in superfused segments of mouse pancreas and salivary glands (sublingual, submaxillary, and parotid glands). Responses of acinar cells in both exocrine pancreas and salivary glands to the neural excitation obtained by field stimulation were similar to responses previously described in each gland to the externally applied acetylcholine. In the pancreatic acinar cell, electrical field simulation induced depolarization with a latency of 0.3 to 1.2 sec. This depolarization was accompanied by a marked decrease in membrane resistance. The equilibrium potential of the depolarization induced by stimulation was between - 10 and - 20 mV. In the sublingual gland, field stimulation induced depolarization of the acinar cell with a latency of 0.2 to 0.3 sec. The stimulus induced depolarization was block by the addition of atropine. In the submaxillary and parotid glands, field stimulation induced depolarization in some acinar cell and hyperpolarization in other cells. The results support evidence previously presented by Petersen and his colleagues that acetylcholine acts to increase Na+ and K+ or Na+, K+, and Cl- permeabilities in the pancreatic acinar cell and to increase K+ and Na+ permeabilities in the salivary gland [11,24].
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D010179:Pancreas / Q000166:cytology / Q000187:drug effects*; D011188:Potassium / Q000378:metabolism; D012469:Salivary Glands / Q000166:cytology / Q000187:drug effects*; D012964:Sodium / Q000378:metabolism
D002712:Chlorides; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium