Facilitation of N-methyl-D-aspartate-evoked acetylcholine release by hydroxyl radical scavengers.

Effects of hydroxyl radical scavengers such as dimethylthiourea (DMTU), uric acid and mannitol on acetylcholine (ACh) release evoked by N-methyl-D-aspartate (NMDA) were examined in cerebral cortical neurones. NMDA increased dose-dependently ACh release. This increase in the release was significantly suppressed by MK-801, N omega-nitro-L-arginine and haemoglobin, indicating that NMDA evokes ACh release via the formation of NO subsequent to NMDA receptor activation. DMTU dose-dependently enhanced the NMDA-induced ACh release. Uric acid (100 microM) and mannitol (1 mM) facilitated significantly the NMDA-induced ACh release, although these scavengers themselves showed no effects on ACh release in the absence of NMDA. These results indicate that the removal of hydroxyl radical facilitates the NO-induced ACh release.