Abstract
1. The amplitude of endplate potentials was increased by concentrations of butanedione monoxime (BDM, 5-20 mM) that typically caused muscle paralysis. 2. Although BDM slowed the decay of spontaneous miniature endplate currents, the effect was insufficient to explain most of the large increase in amplitude of endplate potentials. 3. The quantal content of endplate potentials was increased by BDM in a reversible, concentration-dependent manner. 4. The frequency of miniature endplate potentials was not changed by 10 mM BDM in the presence of normal or raised potassium concentrations, indicating that BDM does not change quantal content by a direct effect on calcium channels or on steady-state intracellular calcium concentration. 5. A change in the time course of the extracellularly recorded nerve terminal action potential caused by BDM was similar to the change produced by 4-aminopyridine (4-AP). 6. The increase in quantal content produced by BDM was only slightly reduced in the presence of 1 mM tetraethylammonium (TEA) but was significantly reduced in the presence of 0.5 to 1 mM 4-AP. 7. It was concluded that BDM blocks a 4-AP-sensitive potassium conductance in motor nerve terminals and, by increasing the duration of the action potential in this way, increases evoked transmitter release.
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Selected References
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- Brigant J. L., Mallart A. Presynaptic currents in mouse motor endings. J Physiol. 1982 Dec;333:619–636. doi: 10.1113/jphysiol.1982.sp014472. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Burley E. S., Jacobs R. S. Effect of 4-aminopyridine on nerve terminal action potentials. J Pharmacol Exp Ther. 1981 Oct;219(1):268–273. [PubMed] [Google Scholar]
- Cooke J. D., Quastel D. M. Transmitter release by mammalian motor nerve terminals in response to focal polarization. J Physiol. 1973 Jan;228(2):377–405. doi: 10.1113/jphysiol.1973.sp010092. [DOI] [PMC free article] [PubMed] [Google Scholar]
- DEL CASTILLO J., KATZ B. Quantal components of the end-plate potential. J Physiol. 1954 Jun 28;124(3):560–573. doi: 10.1113/jphysiol.1954.sp005129. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Fryer M. W., Gage P. W., Neering I. R., Dulhunty A. F., Lamb G. D. Paralysis of skeletal muscle by butanedione monoxime, a chemical phosphatase. Pflugers Arch. 1988 Jan;411(1):76–79. doi: 10.1007/BF00581649. [DOI] [PubMed] [Google Scholar]
- Gage P. W., McBurney R. N. An analysis of the relationship between the current and potential generated by a quantum of acetylcholine in muscle fibers without transverse tubules. J Membr Biol. 1973;12(3):247–272. doi: 10.1007/BF01870004. [DOI] [PubMed] [Google Scholar]
- Li T., Sperelakis N., Teneick R. E., Solaro R. J. Effects of diacetyl monoxime on cardiac excitation-contraction coupling. J Pharmacol Exp Ther. 1985 Mar;232(3):688–695. [PubMed] [Google Scholar]
- Saint D. A., Quastel D. M., Guan Y. Y. Multiple potassium conductances at the mammalian motor nerve terminal. Pflugers Arch. 1987 Nov;410(4-5):408–412. doi: 10.1007/BF00586518. [DOI] [PubMed] [Google Scholar]
- WILSON I. B., GINSBURG B. A powerful reactivator of alkylphosphate-inhibited acetylcholinesterase. Biochim Biophys Acta. 1955 Sep;18(1):168–170. doi: 10.1016/0006-3002(55)90040-8. [DOI] [PubMed] [Google Scholar]
- Wiggins J. R., Reiser J., Fitzpatrick D. F., Bergey J. L. Inotropic actions of diacetyl monoxime in cat ventricular muscle. J Pharmacol Exp Ther. 1980 Feb;212(2):217–224. [PubMed] [Google Scholar]