Lack of protection from ischemic injury of monoamine oxidase B-deficient mice following middle cerebral artery occlusion

Adult male wild-type mice received intraperitoneal (i.p.) administration of saline (n = 9) or 10 mg/kg L-deprenyl (n = 9) three times a week for 3 wee ks. Mice with targeted inactivation of the monoamine oxidase B (MAO-B) gene received i.p. administration of saline (n = 8). Animals underwent ligation of the left common and external carotid arteries, followed by cauterizatio n of the ipsilateral middle cerebral artery. Twenty-four hours post-surgery , all groups showed right torsion of the torso but no evidence of limb weak ness, lateral instability, or circling. Ischemic changes were assessed from digitized video-images of serial sections of the brain stained with Hemato xylin/Eosin. No significant group differences were detected in infarct Volu me (14-18% of ipsilateral cortex) or in the extent of brain edema (4-7% inc rease in ipsilateral hemispheric swelling with respect to contralateral sid e). Our results suggest that absence of the MAO-B gene or inhibition of the enzyme with L-deprenyl are not protective or detrimental in an animal mode l of acute cortical infarction. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.