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.
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+]o in 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.
Brunder
D G
DG
Department of Physiology, School of Medicine, East Carolina University, Greenville, NC 27858.
Lieberman
E M
EM
D000818:Animals; D003400:Astacoidea / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D001369:Axons / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D001693:Biological Transport, Active / Q000187:drug effects; D002034:Bumetanide / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D010277:Parasympathomimetics / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D012964:Sodium / Q000494:pharmacology
D002712:Chlorides; D010277:Parasympathomimetics; D002034:Bumetanide; D005665:Furosemide; D002217:Carbachol; D012964:Sodium; D011188:Potassium