1. Intracellular recordings of membrane potentials have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro-electrodes.2. The mean membrane potential of the acinar cells during superfusion with Krebs-Henseleit solution was -39·2 mV. Increasing [K]o tenfold decreased the membrane potential by 28 mV when [K]o was above 10 mM. This depolarization was not affected by atropine (1·4 × 10-6 M). Strophanthin-G (10-3 M) slowly depolarized the cells at about 10 mV hr-1.3. Brief exposure to acetylcholine (ACh), 5·5 × 10-5 M, or pancreozymin resulted in a short lasting depolarization of the acinar cells. Atropine (1·4 × 10-6 M) blocked the depolarizing action of ACh but not that of pancreozymin. Adrenaline (5·5 × 10-5 M) or cyclic AMP (10-3-10-4 M) did not influence the membrane potential.4. The amplitude of the ACh-induced depolarization was not dependent on the presence of CO2/HCO3 in the bathing fluid, but it was closely dependent on the extracellular Na concentration. However, ACh was still able to evoke a small depolarization even after prolonged exposure of the tissue to a Na-free solution.5. During exposure of the tissue to a Ca-free solution the resting membrane potential was decreased and the ACh-induced depolarization was significantly reduced. Some substances which are known in other tissues to inhibit membrane Ca2+ currents, i.e. La3+, D-600 and tetracaine, were able to reduce, but never abolish, the ACh-induced depolarization.6. These results suggest that the effect of ACh on the pancreatic acinar cell is to increase the permeability of the membrane to commonly occurring ions with a consequent Na-influx and a small Ca-influx.
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