• 1 January 1976
    • journal article
    • research article
    • Vol. 65  (3) , 553-563
Abstract
In contrast to the depolarization observed in hyperosmotic media, exposure of peripheral nerve to hyposmotic conditions induced pronounced axonal hyperpolarization. This hyperpolarization probably resulted from an increased K+ permeability 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 < 665 mosm. Probably, 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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