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1. Intracellular electrodes were used to study the origin of fibrillation potentials in chronically denervated rat muscle. 2. Fibrillation potentials were observed to start from spontaneous biphasic membrane potential oscillations. Each action potential was followed by an after-hyperpolarization which in turn served as a pre-potential for the next spike. The critical level (threshold) for the initiation of the first spike in a train was lower than that of the next and subsequent spikes. 3. A correlation was found between the level of membrane potential and the critical level for action potential generation. This relation was most marked around the resting membrane potential (minus 60 to minus 80 mV) where 10 mV hyperpolarization caused a 9 m V increase in the critical potential level. At higher membrane potentials the correlation was less pronounced. In innervated muscles a similar correlation existed but it was less marked and was present only at membrane polarizations below the resting potential. 4. Increasing the external calcium concentration from 2 to 8 mM reduced the membrane potential-critical level relationship in denervated fibres towards that of innervated ones. 5. As critical level changes with membrane hyperpolarization, the rate of rise of the action potential increased, suggesting a progressive removal of sodium inactivation. 6. It is suggested that a mechanism similar to anode break excitation is important for the induction and maintenance of fibrillation potentials.

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