A study of tetanic and post‐tetanic potentiation of miniature end‐plate potentials at the frog neuromuscular junction.

Abstract

The involvement of Ca, Na, K and Mg in tetanic and post-tetanic potentiation of miniature end-plate potential frequency was examined at the frog neuromuscular junction using conventional electrophysiological techniques. Tetanic potentiation is larger in Ca containing solutions, than in solutions which generate reversed electrochemical gradient for Ca during nerve activity. Tetanic potentiation increases with stimulation frequency and duration, under both inward and reversed electrochemical gradient for Ca conditions. Factors, other than Ca entry apparently participate in tetanic potentiation. Addition of the K conductance blocking agent, 3-aminopyridine (5 mM), increases tetanic potentiation in Ca-containing media, while depressing it under reversed Ca gradient. Electronic depolarization of the nerve terminal in tetrodotoxin-containing Ringer solution produces tetanic potentiation under inward gradient, but fails to do so under reversed gradient. The entry of Na ions apparently participates in the generation of tetanic potentiation. Addition of Mg ions suppresses tetanic potentiation in Ca-containing solution, but increases tetanic potentiation under reversed gradient. Ca entry and intracellular Ca translocation may participate in the generation of tetanic potentiation. Both the fast and the slow components (augmentation and potentiation, respectively) of post-tetanic potentiation increase in duration, with increase in the tetanic stimulation rate. The decay of post-tetanic potentiation increases when [Ca]o [extracellular Ca concentration] is elevated by ionophoretic application during the decay phase only, when ouabain is present in the medium, or when [Mg]o [extracellular Mg concentration] is elevated. Ca, Na and possibly Mg apparently take part in post-tetanic potentiation.