Effects of atropine on the release of newly synthesized acetylcholine from rat striatal slices at various concentrations of calcium ions
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články
PubMed
2325824
DOI
10.1007/bf00969182
Knihovny.cz E-zdroje
- MeSH
- acetylcholin metabolismus MeSH
- atropin farmakologie MeSH
- corpus striatum účinky léků metabolismus MeSH
- inbrední kmeny potkanů MeSH
- krysa rodu Rattus MeSH
- techniky in vitro MeSH
- vápník fyziologie MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- acetylcholin MeSH
- atropin MeSH
- vápník MeSH
The release of acetylcholine (ACh) from brain tissue is known to be inhibited by muscarinic autoreceptors on cholinergic nerve terminals but the mechanism of the inhibition is not understood. Atropine brings about an increase of ACh release by removing the inhibitory action of autoreceptors. We investigated whether the effect of atropine on the release of [14C]ACh newly synthesized during incubations from [U-14C] glucose depends on the concentration of Ca2+ in the medium. In rat striatal slices incubated in the presence of an inhibitor of cholinesterases and of 30 mmol/l K+, significant increases in the release of [14C]ACh elicited by atropine were only observed during incubations with very low concentrations of Ca2+. This finding supports the view that the activation of presynaptic muscarinic autoreceptors in the brain affects the release of ACh by reducing the availability of Ca2+ that is required for transmitter liberation.
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