Monoamine oxidase inhibitors prevent striatal neuronal necrosis induced by transient forebrain ischemia.
Avainsanat
Abstrakti
Seven days after 30 min of ischemia, neuronal necrosis was observed in the striatum. Pretreatment with type A monoamine oxidase (MAO-A) inhibitors, clorgyline and RS-8359 ((+)-4-(4-cyanoanilino)-7-hydroxycyclopenta (3,2-e) pyrimidine) decreased significantly the number of necrotic neurons and inhibited changes in the dopamine metabolite contents during and after transient ischemia. An MAO-B inhibitor, deprenyl also decreased the neuronal necrosis, but it inhibited only the changes in 3,4-dihydroxyphenylacetic acid (DOPAC) content after reperfusion. The results suggest that the activation of dopamine metabolism after transient ischemia was mainly mediated by MAO-A and partly by MAO-B and suggest a possible role of dopamine deamination by MAO in the development of ischemic neuronal necrosis.