Pancreatic acinar cells: ionic dependence of acetylcholine-induced membrane potential and resistance change.
1. Intracellular recordings of membrane potential, input resistance and time constant have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro-electrodes. The acinar cells were stimulated by acetylcholine (ACh). In some cases ACh was simply directly added to the tissue superfusion bath, in other experiments ACh was applied locally to pancreatic acini by micro-iontophoresis. 2. Current-voltage relations were investigated by injecting rectangular de- or hyperpolarizing current pulses through the recording micro-electrode. Within a relatively wide range (-20 to -70 mV) there was a linear relation between injected current and change in membrane potential. The slope of such linear curves corresponded to an input resistance of about 3-8 M omega. The membrane time constant was about 5-10 msec. 3. ACh depolarized the cell membrane and caused a marked reduction of input resistance and time constant. The minimum latency of the ACh-induced depolarization (microiontophoretic application) was 100-300 msec. Maximal depolarization was about 20 mV. The effect of this local ACh application was abolished by atropine (1-4 x 10-6 M). The blocking effect of atropine was fully reversible. 4. Stimulating with ACh during the passage of large depolarizing current pulses made it possible simultaneously to observe the effect of ACh at two different levels of resting potential (RP). At the spontaneous RP of about minus 40 mV ACh evoked a depolarization of usual magnitude (15-20 mV) while at the artificially displaced level of about -10 mV a small hyperpolarization (about 5 mV) was observed. It therefore appears that the reversal potential of the transmitter equilibrium potential is about -20 mV. 5. Replacement of the superfusion fluid C1 by sulphate or methylsulphate caused an initial short-lasting depolarization, thereafter the normal resting potential was reassumed...
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002021:Buffers; D002118:Calcium / Q000494:pharmacology; D002462:Cell Membrane / Q000502:physiology; D002463:Cell Membrane Permeability; D002712:Chlorides / Q000494:pharmacology; D004553:Electric Conductivity / Q000187:drug effects; D005026:Ethylene Glycols / Q000494:pharmacology; D066298:In Vitro Techniques; D007478:Iontophoresis; D008094:Lithium / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008839:Microelectrodes; D010179:Pancreas / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000494:pharmacology; D012996:Solutions; D013431:Sulfates / Q000494:pharmacology
D002021:Buffers; D002712:Chlorides; D005026:Ethylene Glycols; D012996:Solutions; D013431:Sulfates; D001285:Atropine; D008094:Lithium; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium