| First Author | Holschneider DP | Year | 1999 |
| Journal | Neurosci Lett | Volume | 259 |
| Issue | 3 | Pages | 161-4 |
| PubMed ID | 10025583 | Mgi Jnum | J:108038 |
| Mgi Id | MGI:3622879 | Doi | 10.1016/s0304-3940(98)00819-2 |
| Citation | Holschneider DP, et al. (1999) Lack of protection from ischemic injury of monoamine oxidase B-deficient mice following middle cerebral artery occlusion. Neurosci Lett 259(3):161-4 |
| abstractText | 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 weeks. 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 cauterization of the ipsilateral middle cerebral artery. Twenty-four hours post-surgery, all groups showed right torsion of the torso but no evidence of limb weakness, lateral instability, or circling. Ischemic changes were assessed from digitized video-images of serial sections of the brain stained with Hematoxylin/Eosin. No significant group differences were detected in infarct volume (14-18% of ipsilateral cortex) or in the extent of brain edema (4-7% increase in ipsilateral hemispheric swelling with respect to contralateral side). 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 model of acute cortical infarction. |
