AI Article Synopsis
- Arachidonic acid (AA) acts as a reversible inhibitor of muscarinic acetylcholine receptors (mAChRs) and its effects on ligand binding were studied across various receptor types.
- AA inhibited binding to all mAChR subtypes, the beta2-adrenergic receptor, 5-hydroxytryptamine receptor, and micro-opioid receptor, while having no effect on the nicotinic receptor, even at high concentrations.
- The findings suggest that AA significantly impacts multiple G protein-coupled receptors (GPCRs), highlighting the need for further research to understand the inhibition mechanisms involved.
Article Abstract
Arachidonic acid (AA), released in response to muscarinic acetylcholine receptor (mAChR) stimulation, previously has been reported to function as a reversible feedback inhibitor of the mAChR. To determine if the effects of AA on binding to the mAChR are subtype specific and whether AA inhibits ligand binding to other G protein-coupled receptors (GPCRs), the effects of AA on ligand binding to the mAChR subtypes (M1, M2, M3, M4, and M5) and to the micro-opioid receptor, beta2-adrenergic receptor (beta2-AR), 5-hydroxytryptamine receptor (5-HTR), and nicotinic receptors were examined. AA was found to inhibit ligand binding to all mAChR subtypes, to the beta2-AR, the 5-HTR, and to the micro-opioid receptor. However, AA does not inhibit ligand binding to the nicotinic receptor, even at high concentrations of AA. Thus, AA inhibits several types of GPCRs, with 50% inhibition occurring at 3-25 MuM, whereas the nicotinic receptor, a non-GPCR, remains unaffected. Further research is needed to determine the mechanism by which AA inhibits GPCR function.
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| http://dx.doi.org/10.1385/JMN:27:2:185 | DOI Listing |
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