Abstract
Effect of nitric oxide (NO) on striatal acetylcholine (ACh) release induced by N-methyl-D-aspartate (NMDA) was investigated in freely moving rats by means of microdialysis. NMDA caused a significant increase in ACh release in the striatum, which was blocked by the specific NMDA receptor antagonists, (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) and (+)-5-methyl- 10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine hydrogen maleate (MK-801), indicating that agonist-evoked increase in ACh release in the striatum was through an NMDA receptor-mediated mechanism. N G -monomethyl-L-arginine acetate salt (L-NMMA; a NO synthase inhibitor) facilitated NMDA-evoked increase in ACh release, while L-arginine (the precursor of NO) inhibited the ACh release. The increase by L-NMMA of ACh release induced by the NMDA was also blocked by L-arginine. These results suggest that NO induced by NMDA receptor-mediated mechanism in cholinergic neurons may mediate an inhibitory regulation of ACh release.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
