Acetylcarnitine, carnitine and glucose diminish the effect of muscarinic antagonist quinuclidinyl benzilate on striatal acetylcholine content
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
1515917
DOI
10.1016/0006-8993(92)90683-z
PII: 0006-8993(92)90683-Z
Knihovny.cz E-resources
- MeSH
- Acetylcholine metabolism MeSH
- Acetylcarnitine pharmacology MeSH
- Quinuclidinyl Benzilate administration & dosage pharmacology MeSH
- Corpus Striatum drug effects metabolism MeSH
- Glucose pharmacology MeSH
- Hippocampus drug effects metabolism MeSH
- Rats, Inbred Strains MeSH
- Carnitine pharmacology MeSH
- Kinetics MeSH
- Rats MeSH
- Cerebral Cortex drug effects metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acetylcholine MeSH
- Acetylcarnitine MeSH
- Quinuclidinyl Benzilate MeSH
- Glucose MeSH
- Carnitine MeSH
The content of acetylcholine (ACh) in the striatum, brain cortex and hippocampus of rats was lowered 20-180 min after intraperitoneal injection of the muscarinic antagonist quinuclidinyl benzilate (QNB). The depletion of ACh content in the striatum was diminished in animals treated with a single dose of acetyl-L-carnitine, L- or D,L-carnitine, or D-glucose. It is likely that QNB stimulates ACh release by blocking presynaptic muscarinic autoreceptors and that acetylcarnitine, carnitine and glucose support the resynthesis of ACh by increasing the availability of acetylcoenzyme A. They do not have the same consistent effect in the brain cortex and hippocampus; this difference may be related to the lower turnover rate of ACh and to the difference in the anatomical arrangement of cholinergic structures in these parts of the brain.
References provided by Crossref.org
Beta-amyloid and cholinergic neurons