MELATONIN PREVENTS INCREASES IN NEURAL NITRIC-OXIDE AND CYCLIC-GMP PRODUCTION AFTER TRANSIENT BRAIN ISCHEMIA AND REPERFUSION IN THE MONGOLIAN GERBIL (MERIONES-UNGUICULATUS)

While nitric oxide (NO) has been implicated as a mediator of glutamate excitotoxicity after cerebral ischemia/reperfusion, melatonin has bee n reported to inhibit brain NO production by suppressing nitric oxide synthase. The purpose of the present studies was to determine the effe ct of exogenous melatonin administration on NO-induced changes during brain ischemia/reperfusion. Indicators of cerebral cortical and cerebe llar NO production [nitrite/nitrate levels and cyclic guanosine monoph osphate(cGMP)] were used to estimate neural changes after transient bi lateral carotid artery ligation followed by reperfusion in adult Mongo lian gerbils (Meriones unguiculatus). Results show for the first time that melatonin prevents the increases in NO and cGMP production after transient ischemia/reperfusion in frontal cerebral cortex and cerebell um of Mongolian gerbils. The inhibitory effect of melatonin on NO prod uction and its ability to scavenge free radicals and the peroxynitrite anion may be responsible for the protective effect of melatonin on ne uronal structures during transient ischemia followed by reperfusion.