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.

• MeSH
• Acetylcholine metabolism   MeSH
• Chlorides metabolism   MeSH
• Excitatory Postsynaptic Potentials MeSH
• Kinetics MeSH
• Muscle, Skeletal growth & development   innervation   MeSH
• Humans MeSH
• Models, Neurological MeSH
• Motor Neurons metabolism   MeSH
• Neuromuscular Junction growth & development   metabolism   MeSH
• Synaptic Transmission * MeSH
• Nitric Oxide metabolism   MeSH
• Presynaptic Terminals metabolism   MeSH
• Sodium-Potassium-Exchanging ATPase metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Acetylcholine MeSH
• Chlorides MeSH
• Nitric Oxide MeSH
• Sodium-Potassium-Exchanging ATPase MeSH