Nitric oxide increases excitability by depressing a calcium activated potassium current in snail neurons

In gastropods, the interneuronal messenger, nitric oxide (NO), modulates sp ike frequency and synaptic transmission. We have characterized the effect o f NO on ion currents underlying neuronal excitability, using current-clamp and two-electrode voltage-clamp techniques. Identified neurons of the pulmo nate snail, Helix pomatia, respond to the NO donor sodium nitroprusside (SN P) by increasing the firing frequency and decreasing the latency. Voltage-c lamp experiments revealed that SNP or S-nitro-N-acetylpenicillamine (SNAP) depressed the macroscopic outward current, while the control compound N-ace tylpenicillamine (NAP) had no effect. Current voltage curves generated from voltage steps to different membrane potentials ranging from -40 to +180 mV showed an N-shaped outward current. Superfusion of ganglia with Ca2+ free Helix solution abolished the N-shape, indicating the contribution of a Ca2 activated K+ current (I-K,I-Ca). Exposure of neurons to SNP or SNAP dimini shed the N-shape, indicating that NO affects /(K,Ca). The depressing effect of SNP on the outward current was slow and reached steady state in about 5 min. In conclusion, our findings indicate that NO enhances excitability in Helix nervous system by decreasing /(K,Ca). (C) 2000 Elsevier Science Irel and Ltd. All rights reserved.