PMID: 6971693Apr 6, 1981Paper

4-Aminopyridine does not increase m.e.p.p. frequencies at junctions depolarized by potassium

Brain Research
W van der Kloot, K S Madden

Abstract

4-aminopyridine (4-AP) is known to produce large increases in quantal acetylcholine release from stimulated motor nerve terminals. It has been suggested that the drug might act directly on Ca2+ channels to increase Ca2+ influx. This possibility was tested at frog neuromuscular junctions depolarized in elevated [K+]out. The 4-AP did not increase miniature end-plate potential frequencies. Also, 4-AP did not alter the increase in frequency that follows a rise in [Ca2+]out at a depolarized junction. Therefore, under these conditions, 4-AP does not appear to change Ca2+ entry into or elimination from the nerve terminal. The results support the hypothesis that 4-AP acts by lengthening the nerve terminal action potential.

References

Jan 31, 1967·Proceedings of the Royal Society of London. Series B, Containing Papers of a Biological Character·B Katz, R Miledi
Jun 1, 1980·The Journal of Physiology·N B Datyner, P W Gage

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Citations

Nov 1, 1987·Pflügers Archiv : European journal of physiology·D A SaintY Y Guan
Jun 1, 1983·Naunyn-Schmiedeberg's Archives of Pharmacology·V Dolezal, S Tucek
Nov 4, 1982·Brain Research·R Tapia, M Sitges
Jan 1, 1982·Comparative Biochemistry and Physiology. C: Comparative Pharmacology·K Kaila
Dec 1, 1984·Acta Physiologica Scandinavica·K KailaK E Akerman
Dec 22, 2004·The European Journal of Neuroscience·Ruth E BrookeJim Deuchars

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