Abstract: The ischemic effect on brain monoamine concentrations was evaluated in 98 mongolian Gerbils, in which carotid lization was undergone under ether anesthesia and neurologic deficit was evaluated at 0.5, 3 and 24h postligation. Stroke index were calculated for each animal and then the animals were killed by decapitation. Monoamine contents of each hemisphere were estimated by fluorimetric method. It was demonstrated that unilateral common carotid artery ligation resulted in cerebral infarction in 42.9% of animals and led to profound decrease in monoanine concentrations of the brain ipsilateral to the lesion site at 0.5, 3 and 24 h postligation, whereas gerbils which underwent sham operation showed a negligible decrease. When concentrations of monoamine were compared with neurologic deficit, the group with neurologic deficit showed a significant negative correlation. Disorder of the monoamine metabolism found during postischemic period possibly contributes to neurological dysfunction after an ischemic insult.