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Action of Co and Ni at the Frog Neuromuscular Junction

Action of Co and Ni at the Frog Neuromuscular Junction 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). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature New Biology Springer Journals

Action of Co and Ni at the Frog Neuromuscular Junction

Nature New Biology , Volume 245 (141): 2 – Sep 1, 1973

Action of Co and Ni at the Frog Neuromuscular Junction

Nature New Biology , Volume 245 (141): 2 – Sep 1, 1973

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).

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References (11)

Publisher
Springer Journals
Copyright
1973 Nature Publishing Group
ISSN
2058-1092
eISSN
2058-1092
DOI
10.1038/newbio245052a0
Publisher site
See Article on Publisher Site

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).

Journal

Nature New BiologySpringer Journals

Published: Sep 1, 1973

Keywords: life sciences, general

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