Affiliations: [a] Department of Neurology and Stroke Center, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
| [b] Department of Neurology, The Second Clinical Medical College of Jinan University, Shenzhen, China
Correspondence:
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Corresponding author: Jinsheng Zeng, Department of Neurology and Stroke Center, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, No. 58 Zhongshan Road 2, Guangzhou, Guangdong 510080, China. Tel.: +86 20 87755766; Fax: +86 20 87335935; E-mail: [email protected].
Abstract: Backgrounds:Cerebral infarction does not only cause focal injury in the ischemic site, but also secondary non-ischemic damage at the remote areas of nervous system associated with the primary focus. Objective:This study investigated the changes in the spinal cord and ventral root after middle cerebral artery occlusion (MCAO) in cynomolgus monkeys (Macaca fascicularis). Methods:Adult male cynonolgus monkeys (4–5 years, 5.5–7.5 kg) were subjected to MCAO (n = 6) or sham surgery (n = 4). After 12 weeks, spinal cords and the ventral roots were harvested. Morphometric alterations in the spinal cord were detected at C5 and L5 levels via immunofluorescence. The profiles of C5 and L5 ventral roots were displayed by toluidine blue staining and transmission electron microscopic examination. Results:Significant axonal loss in the contralateral corticospinal tract and abnormally enlarged axons in the ipsilateral were observed in monkeys with MCAO. The number of neurons in the contralateral ventral horn got declined while that in the ipsilateral was almost unaffected after MCAO compared with sham controls. Glial activation post-MCAO was observed in the bilateral corticospinal tract and the ventral horn. Aberrant nerve fibers appeared frequently in the contralateral ventral roots of MCAO monkey but rarely in the ipsilateral. Conclusions:These results indicate that focal cerebral infarction leads to pathological alterations in the spinal cord and ventral roots in non-human primates.
