Abstract
The depolarization of crab nerve during repetitive stimulation is unaffected by the presence of glucose or by an increase in the calcium content of the medium. It is increased in both amplitude and rate by veratrine; in the presence of this alkaloid mixture the rate but not the magnitude of the depolarization is increased by an elevation in the calcium concentration. Repolarization following stimulation is unaltered by glucose and accelerated by a greater calcium concentration. Veratrine increases both the amplitude and the time constant of repolarization; its effect on the time constant is counteracted by an elevation of the calcium in the medium. Potassium released during stimulation and its reabsorption following activity have been observed by analyses of small volumes of sea water in contact with crab nerve. Under the conditions employed 3 x 10–8 µM potassium is liberated per impulse per gm. wet weight of nerve. This loss is increased by low concentrations of veratrine, which also increase the amount reabsorbed during recovery. The depletion of potassium from the medium is appreciably less if the potassium previously released during activity has not been removed. Inexcitability resulting from anoxia can be washed away with oxygen-free solution—rapidly and completely in the case of the squid axon, slowly and incompletely in crab nerve. The potassium shifts are in the proper direction and of the correct order of magnitude to account for the negative and positive after-potentials in terms of potassium accumulation or depletion in the extracellular space.
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Selected References
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