Changes in the brain content of biogenic amines constitute one of the main factors implicated in the pathogenesis of ischemic central nervous system damage. We have recently demonstrated a lack of correlation between the cortical ischemic changes of energy related metabolites and noradrenergic metabolites in the adult or the young gerbil brains. This study was extended to the striatum (which is more vulnerable to ischemia than cortex) to further elucidate the relationship between the ischemic cerebral monoamine changes and the lesser susceptibility of young than adult animals to ischemic insult. Bilateral ischemia of 5 to 15 minutes duration with and without 1 hour reflow similarly affected the glucose and energy-related metabolites in both groups of animals. A reduction in striatal norepinephrine (NE) level was only detected in adults after each period of ischemia. In adults, 15 minutes but not 5 minutes of ischemia reduced the striatal dopamine (DA) content which also decreased during recirculation. In young animals, the same striatal DA changes were seen after 15 minutes ischemia with reflow. The delayed alternation of monoamines in the striatum of the young animals observed in reflow but not during ischemia as seen in adults resembles the described maturation"""""""" phenomenon in the adult brain. The late manifestations of monoaminergic changes in young as compared to adult brain structures most likely reflect a lesser intensity of ischemic injury in the young than adult animal. These observations suggest that the relative resistance of young animals to ischemia may be related to the function of neurotransmitters in the central nervous system.
