Effects of tetrodotoxin, Ca2+ absence, d-tubocurarine and vesamicol on spontaneous acetylcholine release from rat muscle
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
1302260
PubMed Central
PMC1175140
DOI
10.1113/jphysiol.1992.sp019402
Knihovny.cz E-resources
- MeSH
- Acetylcholine metabolism MeSH
- Diaphragm MeSH
- Time Factors MeSH
- Depression, Chemical MeSH
- Cholinesterases physiology MeSH
- Denervation MeSH
- Neuromuscular Depolarizing Agents pharmacology MeSH
- Rats MeSH
- Piperidines pharmacology MeSH
- Rats, Wistar MeSH
- Muscles innervation metabolism MeSH
- In Vitro Techniques MeSH
- Tetrodotoxin pharmacology MeSH
- Tubocurarine pharmacology MeSH
- Calcium physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acetylcholine MeSH
- Cholinesterases MeSH
- Neuromuscular Depolarizing Agents MeSH
- Piperidines MeSH
- Tetrodotoxin MeSH
- Tubocurarine MeSH
- Calcium MeSH
- vesamicol MeSH Browser
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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