Inhibitory action of Ca2+ on spontaneous transmitter release at motor nerve terminals in a high K+ solution.
The inhibitory effect of a high external Ca2+ ([Ca2+]o) on spontaneous transmitter release in a high K+ solution (Gage and Quastel 1966; Birks et al. 1968) was studied at the frog neuromuscular junction, based on the hypothesis that an increased intracellular free Ca2+ ([Ca2+]i) in the nerve terminal plays a key role in the depression. Three procedures were employed to increase [Ca2+]i; increasing [Ca2+]o, application of caffeine and tetanic nerve stimulation. All of these procedures increased m.e.p.p. frequency in normal Ringer. However, as the basic m.e.p.p. frequency was increased by raising the external K+ concentration (7--15 mM), their facilitatory effects on m.e.p.p. frequency decreased, dissapeared and eventually reversed to depressant actions. Since a rise in the external K+ concentration would increase the steady state level of [Ca2+]i, it is suggested that when the [Ca2+]i is preset at a high level, manipulations so as to further increase [Ca2+]i depress spontaneous release of transmitter. Possible mechanisms for this inhibition was discussed in relation to a question whether or not the rate of spontaneous transmitter release is a monotonic function of [Ca2+]i.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology / Q000502:physiology*; D003864:Depression, Chemical; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009469:Neuromuscular Junction / Q000378:metabolism / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D011898:Ranidae / Q000502:physiology
D002110:Caffeine; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium