Abstract
The outflux of potassium in metabolizing, desheathed, sciatic nerves of the toad, Bufo marinus, undergoes only a transitory decline upon application of 0.1% cocaine. However, when the outflux has been increased previously by a combination of anoxia and iodoacetate poisoning, cocaine produces a sustained depression of this outflux. These observations seem accounted for qualitatively by the postulate that only the outermost layer of the membrane is affected by the local anesthetic, the permeability to both potassium and sodium being reduced in this restricted region.
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