Electrophysiological and pharmacological properties of glial cells associated with the medial giant axon of the crayfish with implications four neuron-glial cell interactions.

Schwann-like glial cells surrounding the medial giant axon of the crayfish (Procambarus clarkii) were impaled with glass microelectrodes to study their responses to cholinomimetics, cholinergic receptor blockers and ouabain. Axon electrical properties were simultaneously monitored. Glial cells have a low membrane potential compared to the axon; -42 mV and -85 mV, respectively. Acetylcholine, carbachol and nicotine hyperpolarized the glial cells but did not affect the axon steady-state or active membrane potentials. The action of the cholinergics was completely blocked by d-tubocurarine and alpha-bungarotoxin. Ouabain hyperpolarized the glial cell but depolarized the axon. Tubocurarine blocked the ouabain hyperpolarization but not the delayed depolarization of the glia cell or the axon. It is concluded that ouabain causes the release of acetylcholine from the glial cell-axon preparation, inducing the glial hyperpolarization. Studies of the axon-glial cell interaction suggest that a function of the glial cell is to actively modulate the periaxonal potassium concentration on a signal from the axon. Periaxonal potassium can strongly affect axon membrane potential through electrogenic Na transport, modifying axon signalling properties.