Increase in Chloride Permeability of Snail Neurons during High Potassium-induced Hyperpolarization

Abstract

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. 1) The membrane resistance always decreased during both hyperpolarizing responses to high K⁺ (24mM) and ACh (0.1mM). 2) Both hyperpolarizing responses to high K⁺ and ACh were reversed in Cl^--free Ringer to the depolarizing responses. 3) Both hyperpolarizing responses to high K⁺ and ACh were markedly augmented immediately after returning to normal Cl^- from Cl^--free Ringer perfusion. 4) Increase in intracellular Cl^--concentration by a leak from KCl-electrode reversed both hyperpolarizing responses to high K⁺ and ACh. 5) Reversal potential of high K⁺-response was always 10-20mV more positive than that of ACh-response, when measured in normal Ringer perfusion. 6) 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.