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).
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References
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KITA, H., KLOOT, W. Action of Co and Ni at the Frog Neuromuscular Junction. Nature New Biology 245, 52–53 (1973). https://doi.org/10.1038/newbio245052a0
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DOI: https://doi.org/10.1038/newbio245052a0
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