Action of Co and Ni at the Frog Neuromuscular Junction
Abstract
Abstract A GREAT deal of evidence shows that Ca2+ is critically involved in the release of acetylcholine (ACh) from motor nerve terminals1 and in the secretion of a variety of lipid-insoluble hormones and transmitters2. At the frog neuromuscular junction, Sr2+ and Ba2+ can replace Ca2+ (refs 3,4). When the motor nerve is stimulated tetanically in solutions without added Ca2+ or even in solutions containing Mg-EGTA there is an increase in miniature endplate potential (m.e.p.p.) frequency. The increase has been attributed to trace amounts of Ca2+ remaining in the solution outside the nerve terminals5, or to Mg2+ acting as a relatively ineffectual substitute for Ca2+ (ref. 6).