scholarly journals Non-quantal acetylcholine release at the neuromuscular junction

2009 ◽  
pp. 763-784
Author(s):  
F Vyskočil ◽  
AI Malomouzh ◽  
EE Nikolsky
Keyword(s):  
Skeletal Muscles ◽  
Acetylcholine Release ◽  
Chloride Transport ◽  
Motor Nerve ◽  
Basic Research ◽  
Motor Nerve Terminal ◽  
Receptor Desensitization ◽  
Quantal Acetylcholine Release ◽  
Endplate Potentials ◽  
Developing Muscle

There are two principal mechanisms of acetylcholine (ACh) release from the resting motor nerve terminal: quantal and nonquantal (NQR); the former being only a small fraction of the total, at least at rest. In the present article we summarize basic research about the NQR that is undoubtedly an important trophic factor during endplate development and in adult neuromuscular contacts. NQR helps to eliminate the polyneural innervation of developing muscle fibers, ensures higher excitability of the adult subsynaptic membrane by surplus polarization and protects the RMP from depolarization by regulating the NO cascade and chloride transport. It shortens the endplate potentials by promoting postsynaptic receptor desensitization when AChE is inhibited during anti-AChE poisoning. In adult synapses, it can also activate the electrogenic Na+/K+-pump, change the degree of synchronization of quanta released by the nerve stimulation and affects the contractility of skeletal muscles.

scholarly journals Ovalbumin-induced sensitization affects non-quantal acetylcholine release from motor nerve terminals and alters contractility of skeletal muscles in mice

2009 ◽  
Vol 94 (2) ◽  
pp. 264-268 ◽  
Author(s):  
Alexander Y. Teplov ◽  
Sergey N. Grishin ◽  
Marat A. Mukhamedyarov ◽  
Airat U. Ziganshin ◽  
Andrey L. Zefirov ◽  
...  
Keyword(s):  
Skeletal Muscles ◽  
Acetylcholine Release ◽  
Motor Nerve ◽  
Nerve Terminals ◽  
Motor Nerve Terminals ◽  
Quantal Acetylcholine Release

Nicardipine inhibits axon conduction but causes dual changes of acetylcholine release in the mouse motor nerve

1989 ◽  
Vol 67 (12) ◽  
pp. 1493-1498 ◽  
Author(s):  
C. C. Chang ◽  
L. C. Chiou ◽  
L. L. Hwang ◽  
S. J. Hong ◽  
C. Y. Huang
Keyword(s):  
Acetylcholine Receptor ◽  
Neuromuscular Transmission ◽  
Acetylcholine Release ◽  
Motor Nerve ◽  
Neuromuscular Block ◽  
Resting Membrane Potential ◽  
Receptor Desensitization ◽  
End Plate ◽  
Agonist Action ◽  
Release Of Acetylcholine

The effects of nicardipine, a dihydropyridine Ca2+-channel antagonist, on neuromuscular transmission and impulse-evoked release of acetylcholine were compared with those of nifedipine. In the isolated mouse phrenic nerve diaphragm, nicardipine (50 μM), but not nifedipine (100 μM), induced neuromuscular block, fade of tetanic contraction, and dropout or all-or-none block of end-plate potentials. Nicardipine had no significant effect on the resting membrane potential and the amplitude of miniature end-plate potentials but increased the frequency and caused the appearance of large size miniature potentials. The quantal contents of evoked end-plate potentials were increased. In the presence of tubocurarine, however, nicardipine depressed the amplitude of end-plate potentials. The compound nerve action potential was also decreased. It is concluded that nicardipine blocks neuromuscular transmission by acting on Na+ channels and inhibits axonal conduction. Nicardipine appeared to affect the evoked release of acetylcholine by dual mechanisms, i.e., an enhancement presumably by an agonist action on Ca2+ channels, like Bay K 8644 and nifedipine, and inhibition by an effect on Na+ channels, like verapamil and diltiazem. In contrast with its inactivity on the amplitude of miniature end-plate potentials, depolarization of the end plate in response to succinylcholine was greatly depressed. The contractile response of baby chick biventer cervicis muscle to exogenous acetylcholine was noncompetitively antagonized by nicardipine (10 μM), but was unaffected by nifedipine (30 μM). These results may implicate that nicardipine blocks the postsynaptic acetylcholine receptor channel by enhancing receptor desensitization or by a use-dependent effect.Key words: nicardipine, calcium channel antagonists, neuromuscular transmission, acetylcholine release, acetylcholine receptor desensitization.

Acute Late Sepsis Attenuates Effects of a Nondepolarizing Neuromuscular Blocker, Rocuronium, by Facilitation of Endplate Potential and Enhancement of Membrane Excitability In Vitro 

2006 ◽  
Vol 105 (5) ◽  
pp. 968-975 ◽  
Author(s):  
Tomohisa Niiya ◽  
Eichi Narimatsu ◽  
Akiyoshi Namiki
Keyword(s):  
Acetylcholine Release ◽  
Cecal Ligation ◽  
Muscle Membrane ◽  
Membrane Excitability ◽  
Neuromuscular Blockers ◽  
Endplate Potential ◽  
Acetylcholine Sensitivity ◽  
Quantal Acetylcholine Release ◽  
Endplate Potentials

Background Sepsis attenuates the muscle-relaxing effects of nondepolarizing neuromuscular blockers. The authors investigated the effects of acute late sepsis on neuromuscular transmission and neuromuscular actions of rocuronium to clarify the mechanisms by which sepsis attenuates the effects of nondepolarizing neuromuscular blockers. Methods Sepsis was induced by cecal ligation and puncture operation. Endplate potentials, acetylcholine potentials, and electrotonic potentials were recorded from the motor endplates of isolated diaphragms from acute late septic and nonseptic rats. Results (1) Sepsis did not influence the effect of rocuronium to decrease endplate potential amplitude, which was increased by sepsis itself; (2) sepsis facilitated the effect of rocuronium to decrease quantal acetylcholine release, which was increased by sepsis itself; (3) sepsis did not influence the effect of rocuronium to decrease acetylcholine sensitivity, which was decreased by sepsis itself; (4) sepsis decreased critical depolarization, and rocuronium did not influence critical depolarization. Conclusions These results indicate that acute late sepsis facilitates endplate potentials and enhances excitability of the muscle membrane, indicated by a decrease of critical depolarization. It is thought that these elicit the sepsis-induced attenuation of the muscle-relaxing effects of rocuronium.

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