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The direct effects of acetylcholine (ACh) on Na+- or Ca2+-dependent action potentials of curarized sympathetic ganglion cells in bullfrogs were investigated under a condition where membrane depolarization caused by the muscarinic action of ACh was nullified by means of a hyperpolarizing current. ACh decreased the after-hyperpolarization of Na+-action potentials in Ringer's solution, and increased the after-depolarization of Ca2+-action potentials in the isotonic Ca2+ solution. In both solutions, the maximum rates of rise of the spikes were decreased and the slope membrane resistance at the original resting level was increased. The effects of ACh were abolished by atropine. On the other hand, ACh showed no significant effects on action potentials of bullfrog spinal ganglion cells which possessed no synapses. These results suggest that the ion conductance channels for generation of action potentials of sympathetic ganglion cells are under the direct control of transmitters, such as ACh.

THE MUSCARINIC EFFECTS OF ACETYLCHOLINE ON THE ACTION POTENTIAL OF BULLFROG SYMPATHETIC GANGLION CELLS