Potassium distribution and membrane potential of sensory neurons in the leech nervous system

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Abstract
The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech CNS were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using KCL-filled single-barreled microelectrodes. All values are means .+-. SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 .+-. 10.6 mM (n = 40) and the average membrane potential was -47.3 .+-. 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 .+-. 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 .+-. 14.1 mM. With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (.gtoreq. 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (< 3 min) effect but began to change after longer exposure (> 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane 1 depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential. After the return to normal [K+]o there was a sharp increase in aKi, indicating rapid uptake of K+ into the cell. The membrane resistance continued to fall, returning to normal only during the transient, second hyperpolarization. Brief exposures to 10 or 0.2 mM [K+]o during the membrane hyperpolarizations induced potential changes of considerably greater amplitude than those obtained in control measurements. The time course and amplitude of the 1st slow and the 2nd transient membrane hyperpolarization were not affected by replacement of all but 3.6 mM Cl- by SO42- (sulfate-based saline). In solutions containing the cardiac glycoside ouabain (5 .times. 10-4 M), the 1st membrane hyperpolarization remained unchanged and the membrane resistance decreased. The 2nd hyperpolarization was abolished and reversed by ouabain. The increased responsiveness of the membrane potential, the decrease in membrane resistance, and the 1st slow membrane hyperpolarization in low [K+]o result from an increase in the K+ conductance of the cell membrane. The 2nd transient hyperpolarization results from the activation of an electrogenic Na+-K pump, from the decrease of K+ conductance, and an increase in the K+ gradient across the membrane.

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