Slow non-cholinergic excitatory potentials in neurones of the guinea-pig coeliac ganglia.

Intracellular recordings were made from neurones of the coeliac ganglia of the guinea-pig in vitro. In addition to the fast excitatory post-synaptic potential (e.p.s.p.) repetitive stimulation (10-20 Hz, 1-2 s) of the left greater splanchnic nerves elicited a slow depolarization in about 70% of the neurones examined. This depolarization lasted for minutes and was resistant to nicotinic and muscarinic antagonists; it was abolished reversibly in a low-Ca2+, high-Mg2+ solution. The response is henceforth termed non-cholinergic e.p.s.p. In about 10% of the neurones the non-cholinergic e.p.s.p. exhibited a biphasic pattern. The fast as well as the non-cholinergic e.p.s.p. could be effectively induced by stimulation of any of the several nerve trunks that enter the ganglion. Moreover, simultaneous stimulation of two separate nerves resulted in a much larger non-cholinergic e.p.s.p. than could be achieved by stimulation of a single nerve. When the membrane potential was manually clamped, the non-cholinergic e.p.s.p. was associated with an increase of membrane resistance in the large majority of cells tested. Membrane hyperpolarization generally caused an increase in the amplitude of the non-cholinergic e.p.s.p.; a decrease was observed in only a few cells. Subthreshold depolarizations induced by direct intracellular stimulation as well as fast e.p.s.p.s elicited by heterosynaptic nerve stimulation were facilitated during the course of a non-cholinergic e.p.s.p., often resulting in spike discharges. A potentiation of lesser magnitude occurred when the membrane potential was manually clamped during the course of the slow response, indicating that the facilitation may be attributed to both membrane depolarization and increased membrane resistance. These results indicate that the non-cholinergic e.p.s.p. constitutes an integral part of synaptic transmission in coeliac ganglia, and that its function may be to provide a mechanism for increasing the responsiveness of sympathetic neurones to incoming fast e.p.s.p.s.