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Nitric oxide increases excitability by depressing a calcium activated potassium current in snail neurons
A Zsombok1, S Schrofner, A Hermann
1Department of Molecular Neurobiology and Cellular Physiology, Institute of Zoology, University of Salzburg, Hellbrunnerstrasse 34, 5020, Salzburg, Austria.
Abstract:
In gastropods, the interneuronal messenger, nitric oxide (NO), modulates spike frequency and synaptic transmission. We have characterized the effect of NO on ion currents underlying neuronal excitability, using current-clamp and two-electrode voltage-clamp techniques. Identified neurons of the pulmonate snail, Helix pomatia, respond to the NO donor sodium nitroprusside (SNP) by increasing the firing frequency and decreasing the latency. Voltage-clamp experiments revealed that SNP or S-nitro-N-acetylpenicillamine (SNAP) depressed the macroscopic outward current, while the control compound N-acetylpenicillamine (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 Ca(2+) free Helix solution abolished the N-shape, indicating the contribution of a Ca(2+) activated K(+) current (I(K,Ca)). Exposure of neurons to SNP or SNAP diminished the N-shape, indicating that NO affects I(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 I(K,Ca).
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