In contrast to the depolarization observed in hyperosmotic media, exposure of peripheral nerve to hyposmotic conditions induced pronounced axonal hyperpolarization. It is suggested that this hyperpolarization resulted from increased potassium and chloride permeabilities which could assist axonal volume regulation in hyposmotic conditions. The hyperpolarization was readily reversible, but the spike-generating mechanism suffered irreversible damage at hyposmotic concentrations below 665 m-osmoles. It is suggested that this axonal damage contributes to the lethal effects of hyposmotic stress in this crustacean osmoconformer and, possibly, in some euryhaline osmoregulators.

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