Skip to main content
NCBI home page
British Journal of Pharmacology and Chemotherapy logoLink to British Journal of Pharmacology and Chemotherapy
. 1964 Dec;23(3):575–591. doi: 10.1111/j.1476-5381.1964.tb01611.x

The relationship between anticurare activity and time course of the endplate potential; a structure-activity approach

A S Kuperman, M Okamoto
PMCID: PMC1704009  PMID: 14256815

Abstract

A comparison of the effects of several quaternary ammonium ions has been made on the intracellularly recorded endplate potential of curarized frog muscle. The hydroxyanilinium ions usually caused an increase in endplate potential amplitude, a slowing of rate of rise and marked prolongation, but rarely caused spike generation. Contrariwise, tetraethylammonium and triethylphenylammonium consistently caused an increase in both amplitude and rate of rise of the endplate potential but no prolongation; these endplate potentials generated muscle spikes. The results suggest a relationship between rate of rise of the endplate potential and the probability of spike generation. Using the neurally evoked contractile response as a signal of transmitter action, the hydroxyanilinium ions were found to be relatively weak antagonists of tubocurarine at deep levels of curarization, indicating a ceiling effect. There was also a ceiling to the effect of hydroxyaniliniums on endplate potential amplitude. Thus, in the presence of high concentrations of tubocurarine, tetraethylammonium is a more potent anticurare agent than is triethyl(3-hydroxyphenyl) ammonium.

Full text

PDF
575

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. DEL CASTILLO J., KATZ B. On the localization of acetylcholine receptors. J Physiol. 1955 Apr 28;128(1):157–181. doi: 10.1113/jphysiol.1955.sp005297. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. FATT P., KATZ B. An analysis of the end-plate potential recorded with an intracellular electrode. J Physiol. 1951 Nov 28;115(3):320–370. doi: 10.1113/jphysiol.1951.sp004675. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. HUBBARD J. I., SCHMIDT R. F. An electrophysiological investigation of mammalian motor nerve terminals. J Physiol. 1963 Apr;166:145–167. doi: 10.1113/jphysiol.1963.sp007096. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. KOKETSU K. Action of tetraethylammonium chloride on neuromuscular transmission in frogs. Am J Physiol. 1958 Apr;193(1):213–218. doi: 10.1152/ajplegacy.1958.193.1.213. [DOI] [PubMed] [Google Scholar]
  5. KUPERMAN A. S., GILL E. W., RIKER W. F. The relationship between cholinesterase inhibition and drug-induced faciliation of mammalian neuromuscular transmission. J Pharmacol Exp Ther. 1961 Apr;132:65–73. [PubMed] [Google Scholar]
  6. NASTUK W. L., ALEXANDER J. T. The action of 3-hydroxyphenyldimethylethyl-ammonium (tensilon) on neuromuscular transmission in the frog. J Pharmacol Exp Ther. 1954 Jul;111(3):302–328. [PubMed] [Google Scholar]
  7. OTSUKA M., ENDO M. The effect of guanidine on neuromuscular transmission. J Pharmacol Exp Ther. 1960 Mar;128:273–282. [PubMed] [Google Scholar]
  8. RIKER W. F., Jr, WERNER G., ROBERTS J., KUPERMAN A. Pharmacologic evidence for the existence of a presynaptic event in neuromuscular transmission. J Pharmacol Exp Ther. 1959 Feb;125(2):150–158. [PubMed] [Google Scholar]
  9. STANDAERT F. G. THE ACTION OF D-TUBOCURARINE ON THE MOTOR NERVE TERMINAL. J Pharmacol Exp Ther. 1964 Feb;143:181–186. [PubMed] [Google Scholar]
  10. STOVNER J. The anticurare activity of tetraethylammonium (TEA). Acta Pharmacol Toxicol (Copenh) 1958;14(4):317–332. [PubMed] [Google Scholar]
  11. WERNER G. Neuromuscular facilitation and antidromic discharges in motor nerves: their relation to activity in motor nerve terminals. J Neurophysiol. 1960 Mar;23:171–187. doi: 10.1152/jn.1960.23.2.171. [DOI] [PubMed] [Google Scholar]

Articles from British Journal of Pharmacology and Chemotherapy are provided here courtesy of The British Pharmacological Society

RESOURCES