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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 x 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 x 10^-5 M, or pancreozymin resulted in a short lasting depolarization of the acinar cells. Atropine (1·4 x 10^-6 M) blocked the depolarizing action of ACh but not that of pancreozymin. Adrenaline (5·5 x 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.