Effects of tetrodotoxin, Ca2+ absence, d-tubocurarine and vesamicol on spontaneous acetylcholine release from rat muscle
Jazyk angličtina Země Anglie, Velká Británie Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
1302260
PubMed Central
PMC1175140
DOI
10.1113/jphysiol.1992.sp019402
Knihovny.cz E-zdroje
- MeSH
- acetylcholin metabolismus MeSH
- bránice MeSH
- časové faktory MeSH
- chemická deprese MeSH
- cholinesterasy fyziologie MeSH
- denervace MeSH
- depolarizující myorelaxancia farmakologie MeSH
- krysa rodu Rattus MeSH
- piperidiny farmakologie MeSH
- potkani Wistar MeSH
- svaly inervace metabolismus MeSH
- techniky in vitro MeSH
- tetrodotoxin farmakologie MeSH
- tubokurarin farmakologie MeSH
- vápník fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- acetylcholin MeSH
- cholinesterasy MeSH
- depolarizující myorelaxancia MeSH
- piperidiny MeSH
- tetrodotoxin MeSH
- tubokurarin MeSH
- vápník MeSH
- vesamicol MeSH Prohlížeč
1. Rat hemidiaphragms were incubated in a physiological low-K+ medium without stimulation and the amount of acetylcholine (ACh) released was measured radioenzymatically. Cholinesterases were inhibited by paraoxon. 2. In the presence of 1 microM tetrodotoxin (TTX), the amount of ACh released during a 2 h incubation was lowered by 40%. A similar decrease was observed in the absence of Ca2+ and in the presence of 10 microM-d-tubocurarine (dTC). The effects of TTX combined with Ca2+ removal, and of TTX combined with dTC were no greater than those of TTX, dTC or Ca2+ removal alone. TTX and dTC had no effect on the release of ACh from diaphragms 4 days after denervation. 3. The reduction of spontaneous ACh release observed in the presence of TTX or dTC or in the absence of Ca2+ is best interpreted on the assumption that about 40% of the ACh release was due to the impulse activity known to be generated in intramuscular motor nerve branches by the ACh which accumulates after the inhibition of cholinesterases. 4. In the presence of 1 and 10 microM vesamicol (AH5183, 2-(4-phenylpiperidino)-cyclohexanol), the release of ACh was also diminished by approximately 40%. Vesamicol did not augment the inhibition of release produced by TTX or by the omission of Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)
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