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Non-quantal acetylcholine release at the neuromuscular junction
F. Vyskočil, A. I. Malomouzh, E. E. Nikolsky
Jazyk angličtina Země Česko
Typ dokumentu přehledy
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- acetylcholin sekrece MeSH
- chloridy metabolismus MeSH
- excitační postsynaptické potenciály MeSH
- financování organizované MeSH
- kinetika MeSH
- kosterní svaly inervace růst a vývoj MeSH
- lidé MeSH
- modely neurologické MeSH
- motorické neurony sekrece MeSH
- nervosvalové spojení růst a vývoj sekrece MeSH
- nervový přenos MeSH
- oxid dusnatý metabolismus MeSH
- presynaptická zakončení sekrece MeSH
- sodíko-draslíková ATPasa metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- přehledy MeSH
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.
Citace poskytuje Crossref.org
Lit.: 162
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- $a 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.
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