Increase in chloride permeability of snail neurons during high potassium-induced hyperpolarization.
High K+-induced hyperpolarization was recorded intracellularly from the snail neurons, Euhadra subnimbosa, and the ionic mechanism underlying this hyperpolarization was analyzed in comparison with the ACh-induced hyperpolarization of the same cell, the latter known to be Cl(-)-dependent. The membrane resistance always decreased during both hyperpolarizing responses to high K+ (24mM) and ACh (0.1 mM). Both hyperpolarizing responses to high K+ and ACh were reversed in Cl(-)-free Ringer to the depolarizing responses. Both hyperpolarizing responses to high K+ and ACh were markedly augmented immediately after returning to normal Cl- from Cl(-)-free Ringer perfusion. Increase in intracellular Cl(-)-concentration by a leak from KCl-electrode reversed both hyperpolarizing responses to high K+ and ACh. Reversal potential of high K+-response was always 10-20 mV more positive than that of ACh-response, when measured in normal Ringer perfusion. Intracellular Cl(-)-concentration of the cells which were hyperpolarized by high K+ was estimated to be one half of that of the cells which were depolarized by high K+. Above results indicated that the high K+-induced hyperpolarization is due to the permeability increase of the postsynaptic membrane toward Cl-, masking the depolarizing effect of high K+ on the same membrane.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000502:physiology*; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D009474:Neurons / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology*; D012908:Snails
D002712:Chlorides; D000109:Acetylcholine; D011188:Potassium