The Journal of Neurophysiology Vol. 81 No. 3 March 1999, pp. 1428-1431
Copyright ©1999 by the American Physiological Society

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Effect of Hypertonicity on Augmentation and Potentiation and on Corresponding Quantal Parameters of Transmitter Release

Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee 37614-0577

Cheng, Hong and Michael D. Miyamoto. Effect of hypertonicity on augmentation and potentiation and on corresponding quantal parameters of transmitter release. Augmentation and (posttetanic) potentiation are two of the four components comprising the enhanced release of transmitter following repetitive nerve stimulation. To examine the quantal basis of these components under isotonic and hypertonic conditions, we recorded miniature endplate potentials (MEPPs) from isolated frog (Rana pipiens) cutaneous pectoris muscles, before and after repetitive nerve stimulation (40 s at 80 Hz). Continuous recordings were made in low Ca²⁺ high Mg²⁺ isotonic Ringer solution, in Ringer that was made hypertonic with 100 mM sucrose, and in wash solution. Estimates were obtained of m (no. of quanta released), n (no. of functional release sites), p (mean probability of release), and var_s p (spatial variance in p), using a method that employed MEPP counts. Hypertonicity abolished augmentation without affecting potentiation. There were prolonged poststimulation increases in m, n, and p and a marked but transient increase in var_s p in the hypertonic solution. All effects were completely reversed with wash. The time constants of decay for potentiation and for var_s p were virtually identical. The results are consistent with the notion that augmentation is caused by Ca²⁺ influx through voltage-gated calcium channels and that potentiation is due to Na⁺-induced Ca²⁺ release from mitochondria. The results also demonstrate the utility of this approach for analyzing the dynamics of quantal transmitter release.