Monoamines and related enzymes in cerebral cortex and basal ganglia following transient ischemia in gerbils.
The post-ischemic effects on cerebral cortex and basal ganglia monoamine levels and monoamine oxidase (MAO A and B) and catechol-O-methyl transferase (COMT) activities were evaluated in Mongolian gerbils (Meriones unguiculatus) subjected to bilateral common carotid arteries of occlusion for 15 min and reflow for 7 days. Disorders of monoamine metabolism was found in ischemic brain which persisted during the long-term post-ischemia. A rebound increase of norepinephrine and serotonin appeared in early stages (up to 1 h) of post-ischemia both in cerebral cortex and basal ganglia; a rebound increase of dopamine as found only in cerebral cortex. Thereafter, the serotonin level ws enhanced over the control level during the whole post-ischemic period whereas the levels of catecholamines were reduced particularly in basal ganglia. With respect to monoamine content and activities of monoamine degraded enzymes an oscillatory behavior was observed in the post-ischemia. Disorder of the monoamine metabolism found during post-ischemic period possibly contributes to neurological dysfunction after an ischemic insult.
D000818:Animals; D001479:Basal Ganglia / Q000378:metabolism*; D002394:Catechol O-Methyltransferase / Q000032:analysis; D002540:Cerebral Cortex / Q000378:metabolism*; D004298:Dopamine / Q000032:analysis*; D005849:Gerbillinae; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008995:Monoamine Oxidase / Q000032:analysis*; D009638:Norepinephrine / Q000032:analysis*; D012701:Serotonin / Q000032:analysis*; D013997:Time Factors
D012701:Serotonin; D008995:Monoamine Oxidase; D002394:Catechol O-Methyltransferase; D004298:Dopamine; D009638:Norepinephrine