Pancreatic acinar cells: localization of acetylcholine receptors and the importance of chloride and calcium for acetylcholine‐evoked depolarization

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Abstract
Intracellular micro-electrode recordings of acinar cell membrane potential and resistance were made from the mouse pancreas superfused in vitro. Acinar cells under investigation were stimulated by microiontophoretic ACh application from an extracellular AChCl-filled microeleccrode. Passing short-lasting ejecting current pulses through the AChCl-electrode caused acinar cell depolarization when the electrode was in an extracellular position not far (< 50 .mu.m) from an acinus impaled by a KCl micro-electrode. After insertion of the AChCl electrode into a neighbouring acinar cell, electrially coupled to the acinar cell already impaled by the KCl-electrode, ejecting ACh current pulses only affected the membrane potential in a direct electrical manner, whereas there was no sign of an effect of ACh on membrane potential. Replacing extracellular chloride by sulfate caused a marked increase in amplitude of the ACh-evoked depolarization. If the membrane potential was recorded with a KCl electrode, ACh continued to evoke very large depolarizations even after more than 1 h exposure to Cl-free solution. If the membrane potential was recorded with a K-citrate electrode the effect of Cl--removal was only transient. Removal of Na+ during exposure to Cl--free solution somewhat reduced the amplitude of the ACh-evoked depolarization. Readmission of Cl- after more than 1 h of Cl- deprivation caused an immediate reversal of the ACh effect into a hyperpolarization. Removal of extracellular Ca2+ caused a marked reduction in amplitude of small depolarizations evoked by just suprathreshold ACh doses, whereas there was very little effect on larger depolarizations evoked by maximal or supramaximal ACh ejections. The effect of Ca2+ removal was fully reversible. Addition of Mn1+ after Ca2+-deprivation was as efficient as Ca2+ in restoring normal electrophysiological responses to small ACh doses. The acinar cell membrane seems only to be responsive to ACh added to the extracellular side, and ACh probably caused an increase in membrane Cl permeability in addition to previously described effects on Na+ and K+ permeability. Ca2+ may be important in determining ACh receptor sensitivity.