On the role of mitochondria in transmitter release from motor nerve terminals.
1. The changes in transmitter release produced by mitochondrial inhibitors has been studied at the frog neuromuscular junction using conventional electrophysiological techniques for stimulation and intracellular recording. 2. Inhibitors of the electron transport chain and inhibitors of oxidative phosphorylation produce an increase in the frequency of appearance of the miniature end-plate potentials. This increase in frequency is observed also in calcium-free media. Mitochondrial inhibitors also augment the amount of transmitter liberated by a nerve impulse. 3. Ruthenium red, which is an inhibitor of calcium uptake by mitochondria, increases the spontaneous transmitter release but decreases the quantal content. The latter effect of Ruthenium red is antagonized by calcium. 4. The mitochondrial content of the motor nerve terminals is, on the average, 6.59%. 5. The experimental results are explained on the hypothesis that spontaneous release of transmitter reflects the resting level of intracellular free calcium and the evoked release reflects the sum of the resting calcium and the calcium brought in by the action potential. The mitochondria play a role in transmitter release by participating in the regulation of the intracellular free Ca.
D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism; D001728:Dicumarol / Q000494:pharmacology; D004594:Electrophysiology; D006146:Guanidines / Q000494:pharmacology; D066298:In Vitro Techniques; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009046:Motor Neurons / Q000502:physiology*; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology; D011894:Rana pipiens; D012428:Ruthenium / Q000494:pharmacology; D009435:Synaptic Transmission / Q000187:drug effects
D006146:Guanidines; D001728:Dicumarol; D012428:Ruthenium; D002118:Calcium