Presynaptic effects of 4-aminopyridine and streptomycin on the neuromuscular junction

Enomoto, Koh-ichi; Maéno, Takashi

doi:10.1016/0014-2999(81)90002-9

Cited by 13 publications

(5 citation statements)

References 43 publications

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“…Aminoglycoside antibiotics are a class of large polycationic amino sugars (Berdy et al, 1980). A body of evidence shows that the aminoglycosides inhibit neuromuscular transmission (Timmerman et al, 1959;Dretchen et al, 1972;Wright and Collier, 1977;Singh et al, 1979;Caputy et al, 1981;Enomoto and Maeno, 1981;Fieckers, 1983). While these drugs are thought to inhibit neurotransmission by blocking voltage-gated Ca 2+ channels, they also block currents through a wide variety of ionic channels, including high-conductance CaZ+-activated K + channels (Nomura et al, 1990), mechanotransduction channels in cochlear and vestibular hair cells (Ohmori, 1985;Kroese et al, 1989;Dulon et al, 1989), as well as voltage-gated Ca 2+ channels (Hint et al, 1982;Suarez-Kurtz and Reuben, 1987;Atchison et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Block of single L-type Ca2+ channels in skeletal muscle fibers by aminoglycoside antibiotics.

Haws

Winegar

Lansman

1996

The Journal of General Physiology

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ABSTRACX The activity of single L-type Ca 2+ channels was recorded from cell-attached patches on acutely isolated skeletal muscle fibers from the mouse. The experiments were concerned with the mechanism by which aminoglycoside antibiotics inhibit ion flow through the channel. Aminoglycosides produced discrete fluctuations in the single-channel current when added to the external solution. The blocking kinetics could be described as a simple bimolecular reaction between an aminoglycoside molecule and the open channel. The blocking rate was found to be increased when either the membrane potential was made more negative or the concentration of external permeant ion was reduced. Both of these effects are consistent with a blocking site that is located within the channel pore. Other features of block, however, were incompatible with a simple pore blocking mechanism. Hyperpolarization enhanced the rate of unblocking, even though an aminoglycoside molecule must dissociate from its binding site in the channel toward the external solution against the membrane field. Raising the external permeant ion concentration also enhanced the rate of unblocking. This latter finding suggests that aminglycoside affinity is modified by repulsive interactions that arise when the pore is simultaneously occupied by a permeant ion and an aminoglycoside molecule.

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Section: Introductionmentioning

confidence: 99%

Block of single L-type Ca2+ channels in skeletal muscle fibers by aminoglycoside antibiotics.

Haws

Winegar

Lansman

1996

The Journal of General Physiology

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“…First, the facilitation of the fast EPSP was not affected by TEA, which is thought to block voltage-dependent K+ channels and raise Ca 21 influx, but is significantly depressed during the ALTP . Second, the magnitude of the ALTP was smaller at relatively high rates of evoked release in normal Ringer or in the presence of TEA than it was at low rates of release in low-Ca 2+ solutions, whereas the treatment with K+ channel blockers (TEA or 4-aminopyridine) caused a significant potentiation of transmitter release even at a high level of release (in normal Ringer : Heuser et al ., 1979;Akasu and Yamada, 1980;Maeno, 1980 ;Enomoto and Maeno, 1981). Third, synaptic delay was not altered during the ALTP, although it was significantly prolonged by various K+ channel inhibitors.…”

Section: K+ Conductance Inactivation Mechanismmentioning

confidence: 93%

Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

Kumamoto¹,

Kuba²

1986

The Journal of General Physiology

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A mechanism of the long-term potentiation of transmitter release induced by adrenaline (ALTP) was studied by recording intracellularly the fast excitatory postsynaptic potentials (fast EPSPs) . The ALTP was produced during the blockade of K+ channels at the presynaptic terminals by tetraethylammonium (TEA). The synaptic delay, possibly reflecting a relative change in the duration of an action potential at the presynaptic terminal, was not changed during the course of the ALTP . By contrast, it was significantly lengthened by TEA and other K+ channel inhibitors (4-aminopyridine and Cs') that markedly enhanced the evoked release of transmitter . The magnitude of facilitation of the fast EPSP, induced by a conditional stimulus to the preganglionic nerve, was decreased during the generation of the ALTP, but was unchanged during the potentiation of transmitter release caused by TEA. These results, together with theoretical considerations applying the residual Ca t`hypothesis to the facilitation, suggest that the enhancement of transmitter release during the ALTP is not caused by an increased Ca" influx during a presynaptic impulse owing to the blockade of K+ channel or the modulation of Ca" channel, but presumably is induced by a rise in the basal level of free Ca" in the presynaptic terminal .

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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: 97%

4-Aminopyridine Hydrochloride (Pymadin)

Paskov¹,

Ágoston²,

Bowman³

1986

New Neuromuscular Blocking Agents

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Presynaptic effects of 4-aminopyridine and streptomycin on the neuromuscular junction

Cited by 13 publications

References 43 publications

Block of single L-type Ca2+ channels in skeletal muscle fibers by aminoglycoside antibiotics.

Block of single L-type Ca2+ channels in skeletal muscle fibers by aminoglycoside antibiotics.

Mechanism of long-term potentiation of transmitter release induced by adrenaline in bullfrog sympathetic ganglia.

4-Aminopyridine Hydrochloride (Pymadin)

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