Role of cyclic nucleotides in effects of hydrogen sulfide on the mediator release in frog neuromuscular junction

The role of cyclic nucleotides in the effects of hydrogen sulfide (H2S) on transmitter release in the frog neuromuscular junction was studied using focal microelectrode recording of synaptic signals. A donor of H2S, sodium hydrogen sulfide (NaHS) (100 µM) reversibly increased the amplitude and quantum content of end-plate currents (EPCs) without changing the nerve ending response. The effect of H2S on evoked transmitter release was decreased by preliminary application of the membrane-permeable cAMP analogue pCPT-cAMP (100 µM). Inhibition of adenylate cyclase by MDL-12330A (0.8 µM) did not alter the effect of NaHS on transmitter release. Membrane-permeable cGMP analogue pCPT-cGMP (50 µM) and inhibitor of guanylate cyclase ODQ (0.1 µM) did not change the effect of NaHS. Therefore, we conclude that the H2S-induced increase in the transmitter release was not a result of guanylate cyclase activity. It was concluded that the H2S effects are related to the functioning of cAMP-dependent mechanisms; however, these effects are not associated with the direct action of H2S on the adenylate cyclase activity.