Early postdenervation depolarization is controlled by acetylcholine and glutamate via nitric oxide regulation of the chloride transporter
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem, přehledy
PubMed
12675147
DOI
10.1023/a:1022833709448
Knihovny.cz E-zdroje
- MeSH
- acetylcholin fyziologie MeSH
- chloridy metabolismus MeSH
- denervace svalu * MeSH
- elektrofyziologie MeSH
- kosterní svaly fyziologie MeSH
- kyselina glutamová fyziologie MeSH
- oxid dusnatý metabolismus MeSH
- transportní proteiny fyziologie MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Názvy látek
- acetylcholin MeSH
- chloridy MeSH
- kyselina glutamová MeSH
- oxid dusnatý MeSH
- transportní proteiny MeSH
Resting non-quantal acetylcholine (ACh) and probably glutamate (Glu) release from nerve endings activates M1- and NMDA receptor-mediated Ca2+ entry into the sarcoplasm with following activation of NOS and production of NO. This is a trophic message from motoneurons, which keeps the Cl- transport inactive in the innervated sarcolemma. After denervation, the secretion of ACh and Glu at the neuromuscular junction is eliminated within 3-4 h and the production of NO in the sarcoplasm is lowered. As a result, the Cl- influx is probably activated by dephosphorylation of the Cl- transporter with subsequent elevation of intracellular Cl- concentration. The equilibrium Cl- potential becomes more positive and the muscle membrane becomes depolarized.
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