Effect of the endogenous analgesic dipeptide, kyotorphin, on transmitter release in sympathetic ganglia.

The effects of kyotorphin and the synthetic analogue, D-kyotorphin, on cholinergic fast excitatory postsynaptic potentials (fast-e.p.s.ps) were studied using intracellular recordings from bullfrog sympathetic ganglion cells. Kyotorphin and D-kyotorphin (1-100 microM) increased the amplitude and the mean quantal content of the fast-e.p.s.p. without changing the mean quantal size in a low Ca2+/high Mg2+ medium. Kyotorphin and D-kyotorphin (1-100 microM) did not change the resting membrane potential, input membrane resistance, the amplitude and duration of action potentials and the sensitivity to the transmitter, acetylcholine (ACh), of the ganglion cells. The facilitatory effect of D-kyotorphin on the fast-e.p.s.p. was reversibly inhibited by naloxone (10 microM). These results indicate that kyotorphin may increase transmitter release from preganglionic nerve terminals. The possible mechanisms underlying this action of kyotorphin are discussed.