Calcium independence of slow currents underlying spike frequency adaptation.
This study assessed the role of calcium in the activation of the slow potassium current responsible for spike frequency adaptation in molluscan neurons. Inward calcium currents were eliminated by using Co2+, Cd2+, or OCa2+ EGTA in the bathing solution. In each case adaptation was found to persist, as did the slow current believed to be responsible for adaptation. Injection of EGTA into neurons was also found not to block adaptation. This potassium current provides an example of a slow voltage-dependent potassium process which is independent of calcium influx.
D000200:Action Potentials / Q000187:drug effects; D000222:Adaptation, Physiological; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002463:Cell Membrane Permeability / Q000187:drug effects; D003035:Cobalt / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D005724:Ganglia / Q000502:physiology*; D006372:Helix, Snails / Q000502:physiology*; D008195:Lymnaea / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology
D002104:Cadmium; D003035:Cobalt; D004533:Egtazic Acid; D009532:Nickel; D002118:Calcium