Abstract
Experiments performed on the denervated gracilis anterior of the rat in situ have shown that fibrillation potentials originate from the denervated endplate zones. Extracellularly recorded potentials show a polarity shift in these areas only. Intra-cellularly recorded fibrillation action potentials are preceded by a slowly rising depolarization (prepotentials) when transmembrane recording is done in this area. In other regions of the muscle fibers fibrillation action potentials take off abruptly from the baseline. Weak cathodal currents increase fibrillation frequency while anodal currents of similar magnitude have the opposite effect only when applied at or near the denervated endplate zones. In other areas of the muscle, similar applications of current do not change fibrillation frequency. Drugs, such as acetylcholine and noradrenaline increase fibrillatory activity only when applied to the denervated endplate zone. Decamethonium blocks fibrillation mainly when applied on the same area. Curare and an excess of either Mg or Ca ions do not change fibrillation frequency.

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