Reversal of streptomycin induced blockade of neuromuscular transmission by 4-aminopyridine.

Maéno, Takashi; Enomoto, Koichi

doi:10.2183/pjab.56.486

Cited by 9 publications

(4 citation statements)

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“…These findings agree with results obtained in the mouse diaphragm with streptomycin (Singh, Marshall and Harvey, 1979) and amikacin (Singh, Marshall and Harvey, 1978a) and in the rat hemidiaphragm preparation with neomycin and gentamicin (Elmqvist and Josefsson, 1962;Caputy, Kim and Sanders, 1981). The effects of altering the external Ca 2+ concentration on the neuromuscular blockade induced by the aminoglycosides were similar to the effects on Mg 2+ -induced blockade, confirming the suggestion that the aminoglycosides reduce transmitter release by a mechanism similar to that of Mg 2 * involving a competition for Ca 2+ binding sites on the nerve terminal (Prado, Corrado and Marseillan, 1978;Maeno and Enomoto, 1980). The effects of streptomycin on m.e.p.p.…”

Section: Discussionmentioning

confidence: 63%

“…Two types of experiment to assess effects on quantal content were performed: in normal frog Ringer solution in which transmitter release was not impaired by other drugs, and in high magnesium Ringer solution in which evoked transmitter release had been reduced to a low level. In addition, it is known that aminoglycosides exert their prejunctional blqpking action by competing with calcium ions for sjfes on the nerve terminal in a manner similar to magnesium ions (Elmqvist and Josefsson, 1962;Prado, Corrado and Marseillan, 1978;Maeno and Enomoto, 1980). Therefore, in the present study we have attempted to assess if the effects of the other three classes of antibiotic tested are a result of a similar competition with calcium ions by examining the effects of the antibiotics on end-plate potential quantal content at four different calcium concentrations.…”

Section: Intracellular Recordingmentioning

confidence: 99%

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Pre- And Postjunctional Blocking Effects of Aminoglycoside, Polymyxin, Tetracycline and Lincosamide Antibiotics

Singh

Marshall

Harvey

1982

British Journal of Anaesthesia

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The effects of seven antibiotics (streptomycin, amikacin, polymyxin B, lincomycin, clindamycin, tetracycline and oxytetracycline) were compared with those of magnesium, tubocurarine and lignocaine in the frog sciatic nerve--sartorius muscle preparation, using intracellular recording techniques. All compounds except tubocurarine decreased end-plate potential quantal content. The prejunctional effects of magnesium, streptomycin, amikacin, polymyxin B and oxytetracycline (but not the other drugs) were well reversed by increasing the calcium concentration. At concentrations which depressed quantal content, only magnesium, tetracycline and oxytetracycline did not reduce postjunctional sensitivity. Further postjunctional effects of the drugs were revealed by alterations in the time-courses of end-plate potentials. All the drugs tested except magnesium, tubocurarine and lincomycin produced changes in muscle action potentials. None of the compounds had anticholinesterase activity. The results confirm that aminoglycoside, polymyxin, tetracycline and lincosamide antibiotics produce neuromuscular block by a combination of both pre- and postjunctional actions.

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Section: Discussionmentioning

confidence: 63%

Section: Intracellular Recordingmentioning

confidence: 99%

Pre- And Postjunctional Blocking Effects of Aminoglycoside, Polymyxin, Tetracycline and Lincosamide Antibiotics

Singh

Marshall

Harvey

1982

British Journal of Anaesthesia

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“…The purpose of the present investigation was to elucidate the kinetics of the direct action of 4AP on the mechanism of transmitter release and the antagonistic interaction of SM thereupon by calculating the fractional release from the store of available ACh quanta (P) from the tetanic rundown of endplate potentials (EPPs) during short train stimulations. Some of the data has already been published in preliminary form (MAENO, 1980;MAENO and ENOMOTO, 1980 (1)…”

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confidence: 99%

Kinetic analysis of the action of chemical modulators on neuromuscular transmission.

1981

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The kinetics of the direct action of 4-aminopyridine (4AP) and streptomycin (SM) on the mechanism of transmitter release were studied by recording the endplate potentials from curarized frog muscles using conventional microelectrode techniques, and by calculating the fractional release from the store of available acetylcholine quanta from the experiments with tetanic rundown during short train stimulations. To explain the tremendous facilitatory effect of 4AP on the fractional release and the antagonistic interaction of SM thereupon, it was postulated that 4AP and SM modify the transmitter output by combining with the Ca-dependent process X; i.e., 4AP and SM compete for the occupancy of the X site. A combination of 4AP or SM presumably modifies allosterically the action of the Ca-X complex, resulting in a profound augmentation of the evoked release of the available transmitter with the former and its depression with the latter. The theoretically derived equations from the above assumptions agreed reasonably well with the results obtained. Aminopyridines have long been known to have a variety of actions on physiological functions. They have been shown to reduce the K conductance of the axonal membrane, exert an anticurare action on the neuromuscular junction (SoBEK et al., 1968 ; BOWMAN et al., 1977 ; HARVEY and MARSHALL, 1977), increase catecholamine release in a variety of tissues, stimulate respiratory activity (FASTIER and MC-DOWALL, 1958), and produce strychnine-like convulsions (FASTIER and MCDOWALL 1958 ; HARVEY and MARSHALL, 1977). The amplitude of the twitch tension of a muscle fiber is potentiated by these compounds (FASTIER and MCDOWALL, 1958 ; BOWMAN et al., 1977 ; HARVEY and MARSHALL, 1977). In particular, 4-aminopyridine (4AP) and 3,4-diaminopyridine (34DAP) have a profound effect on the neuromuscular junction. By enhancing enormously the release of transmitter from the motor nerve terminal (DURANT and MARSHALL, 1980), 4AP and 34DAP antagonize the d-tubocurarine (dTC) and antibiotic-induced neuromuscular blockades, and also relieve the long-lasting muscle paralysis produced by Botulinum

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“…myasthenia gravis, tubocurarine paralysis). Certainly, 4-aminopyridine seems to be a better antagonist of antibiotics that block transmission predominantly by a prejunctional mechanism (aminoglycosides, polymyxins) than of those that act by a post junctional mechanism (tetracyclines, certain lincosamides) (SOBEK et al 1968;SINGH et al 1978 a, b;LEE et al 1978;MAENO and ENOMOTO 1980;ENOMOTO and MAENO 1981;UCHIYAMA et al 1981;DURANT and LAMBERT 1981). Aminopyridines are also very effective against the depression of transmitter release in experimental botulism LUNDH 1978b;TAZIEFF-DEPIERRE et al 1978;SIMPSON 1978;MOLGO et al 1980), or that produced by crotoxin (VITAL-BRAZIL et al 1979).…”

Section: Repetitive Nerve Stimulationmentioning

confidence: 99%

4-Aminopyridine Hydrochloride (Pymadin)

Paskov¹,

Ágoston²,

Bowman³

1986

New Neuromuscular Blocking Agents

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Reversal of streptomycin induced blockade of neuromuscular transmission by 4-aminopyridine.

Cited by 9 publications

References 0 publications

Pre- And Postjunctional Blocking Effects of Aminoglycoside, Polymyxin, Tetracycline and Lincosamide Antibiotics

Pre- And Postjunctional Blocking Effects of Aminoglycoside, Polymyxin, Tetracycline and Lincosamide Antibiotics

Kinetic analysis of the action of chemical modulators on neuromuscular transmission.

4-Aminopyridine Hydrochloride (Pymadin)

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