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MAO‐B Inhibition by a Single Dose of l‐Deprenyl or Lazabemide Does Not Prevent Neuronal Damage Following Focal Cerebral Ischaemia in Rats
Author(s) -
Jolkkonen Jukka,
Kauppinen Risto,
Nyman Leena,
Haapalinna Antti,
Sivenius Juhani
Publication year - 2000
Publication title -
pharmacology & toxicology
Language(s) - English
Resource type - Journals
eISSN - 1600-0773
pISSN - 0901-9928
DOI - 10.1034/j.1600-0773.2000.pto870509.x
Subject(s) - ischemia , monoamine oxidase , striatum , pharmacology , monoamine oxidase b , medicine , oxidative stress , monoamine oxidase a , cerebral cortex , cortex (anatomy) , chemistry , anesthesia , dopamine , enzyme , biochemistry , biology , neuroscience
The present study investigated the effect of postischaemic infusion of an irreversible monoamine oxidase B (MAO‐B) inhibitor, l‐deprenyl, an equipotent dose of a reversible MAO‐B inhibitor, lazabemide, or 0.9% NaCl on infarct volumes following focal cerebral ischaemia in rats. The drug doses (0.3 mg/kg) were selected to induce selective MAO‐B inhibition (45–55%), but not MAO‐A inhibition. The infarct volumes in the cortex or in the striatum did not differ between the experimental groups 72 hr after transient occlusion of the middle cerebral artery, which suggests that during ischaemia/reperfusion, suppressed oxidative stress by partial MAO‐B inhibition or MAO‐B independent mechanisms such as induction of trophic factors, does not protect against ischaemia/reperfusion damage.

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