Dun_1981_J.Pharmacol.Exp.Ther_217_714

Effects of 5-hydroxytryptamine (5-HT) on synaptic transmission of isolated rabbit superior cervical ganglia were investigated by means of intracellular recording techniques. Superfusion of 5-HT (1-100 microM) onto the ganglion cells reversibly depressed the amplitude of the fast excitatory postsynaptic potential (epsp) without causing a noticeable change in the membrane potential or input resistance in the majority of cells studied. In a portion of neurons, 5-HT produced a small to moderate, transient depolarization accompanied by a fall in membrane resistance, as well as a diminution of the epsp. In these neurons, the synaptic potentials did not recover to their full amplitude even when the membrane potentials and membrane resistance had returned to the control level. The inhibitory effect of 5-HT was not antagonized by lysergic acid diethylamide (0.3-1 microM), methysergide (1-10 microM), picrotoxin (10-50 microM) and phenoxybenzamine (5 microM); the first two agents when applied alone reversibly diminished the epsp. The mean quantal content but not the quantal size of the evoked epsp was significantly reduced by 5-HT in a low Ca/high Mg solution. Lastly, 5-HT reduced the amplitude of epsp while not appreciably affecting the acetylcholine potential induced by iontophoresis of the acetylcholine onto the same ganglion cells. These results provide electrophysiological evidence suggesting that 5-HT-induced inhibition of synaptic transmission in sympathetic ganglia is primarily due to a presynaptic mechanism resulting in a reduction of the evoked release of acetylcholine.