Non-quantal acetylcholine release at the neuromuscular junction.
There are two principal mechanisms of acetylcholine (ACh) release from the resting motor nerve terminal: quantal and non-quantal (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.
Vyskocil
F
F
Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic. vyskocil@biomed.cas.cz
Malomouzh
A I
AI
Nikolsky
E E
EE
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002712:Chlorides / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials; D006801:Humans; D007700:Kinetics; D008959:Models, Neurological; D009046:Motor Neurons / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000254:growth & development / Q000294:innervation*; D009469:Neuromuscular Junction / Q000254:growth & development / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D017729:Presynaptic Terminals / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D009435:Synaptic Transmission
D002712:Chlorides; D009569:Nitric Oxide; D000254:Sodium-Potassium-Exchanging ATPase; D000109:Acetylcholine