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

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• 作者：Zsombok ; Andrea ; Schrofner ; Siegfried ; Hermann ; Anton ; Kerschbaum ; Hubert H.
• 关键词：Nitric oxide ; Gastropods ; Invertebrate ; Neuron ; Excitability ; Ion currents
• 刊名：Neuroscience Letters
• 出版年：2000
• 出版时间：December 8, 2000
• 年：2000
• 卷：295
• 期：3
• 页码：85-88
• 全文大小：152 K

文摘

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 Ca²⁺ free Helix solution abolished the N-shape, indicating the contribution of a Ca²⁺ 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.