Zinc modulates A-type potassium currents and neuronal excitability in snail neurons.
1. Zinc-induced actions were studied on the A-current and neuronal activity in identified and unidentified nerve cells of the snail, Helix pomatia, L., under voltage and current clamp conditions. 2. Extracellularly applied Zn2+ attenuated the peak amplitude of the A-current in a potential- and dose-dependent way (Ki = 1.8 mM at -30 mV, nH = 0.6). 3. Attenuation of the A-currents was initiated as Zn2+ shifted the potential dependence of both activation and inactivation of the currents toward more positive potential values. 4. Zinc concomitantly prolonged the time to peak and the decay time constant of the A-currents (Kd = 1.7 mM, nH = 1.4) as well. 5. Zn2+ decreased the resting membrane potential and the spike amplitude and increased the action potential duration and the input resistance of the cells in current clamp experiments. 6. A complex action of zinc increased the neuronal excitability, indicating spontaneous and synaptically evoked spike discharges. 7. Common and specific zinc binding sites are supposed on vertebrate and invertebrate A-type potassium channel proteins, where binding Zn2+ can modulate the gating properties and kinetics of the fast outward potassium currents.
Erdélyi
L
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Department of Comparative Physiology, József Attila University of Sciences, Szeged, Hungary.
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D017952:Ganglia, Invertebrate / Q000502:physiology; D006372:Helix, Snails; D007448:Invertebrates; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D014714:Vertebrates; D015032:Zinc / Q000494:pharmacology*
D015220:Calcium Channels; D015221:Potassium Channels; D015032:Zinc