Studies of axon-glial cell interactions and periaxonal K + homeostasis—I. The influence of Na +, K +, Cl − and cholinergic agents on the membrane potential of the adaxonal glia of the crayfish medial giant axon

Abstract

The ionic basis for the low (− 40 mV) resting membrane potential of glial cells surrounding the giant axons of the crayfish and their hyperpolarization by cholinergic agents (to − 55 mV) was studied using standard electrophysiological techniques, ionic substitutions and pharmacological agents. The resting membrane potential of the glial cell was depolarized by increasing [ K +] o, but the response was not Nernstian. Na + depletion caused a small depolarization of the glial resting membrane potential, whereas Cl − depletion resulted in a hyperpolarization comparable to that seen with carbachol at various [ K +] o. Both furosemide (1 mM) and bumetanide (0.1 mM) produced an 8–10 mV hyperpolarization as compared to 15–17 mV seen with Cl − depletion or carbachol. Carbachol has no further effect on the potential following furosemide treatment or Cl − depletion. After carbachol administration or Cl − depletion the resting membrane potential of the glial cell responded to [ K +] oin a more Nernstian manner. The data indicate that the low resting membrane potential of glial cells is due to a combination of a low [ K +] i and an outwardly-directed (depolarizing) Cl − electrochemical gradient. Carbachol acts to decrease Cl − conductance, resulting in the hyperpolarization of the glial cell membrane and a decrease in the outwardly-directed K + electrochemical gradient by approximately two-thirds. We hypothesize that this mechanism for modulation of the glial cell membrane potential and the K + electrochemical gradient serves to enhance the uptake of K + by the glial cell transport system.