Photochemically induced cerebral ischemia in a mouse model

Photochemically induced cerebral ischemia in a mouse model
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DOI:
10.1016/j.surneu.2006.08.077
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发表时间:
2007-06-01
期刊:
影响因子:
--
通讯作者:
Kim, Soo-Han
Kim, Soo-Han
中科院分区:
其他
文献类型:
--
作者:
Lee, Jung-Kil;Park, Min-Sung;Kim, Soo-Han

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背景:MCAO已被广泛用于产生缺血性脑损伤。MCAO引起的病变往往是可变的大小,因为在小鼠brain.Methods中发现的侧支血供的方差:我们修改了大鼠光血栓形成模型用于小鼠。雄性C5713 L/6小鼠通过皮质微血管光血栓形成造成局灶性脑缺血。通过腹腔内注射虎红(一种光敏染料)和通过颅骨局部照射来产生脑梗死。通过加速旋转杆和楼梯测试评估运动障碍。结果:脑梗死灶位于额叶和顶叶皮质,基底白色物质部分受累。一个相对恒定的梗死体积,实现了一个月后光血栓形成。光血栓病变的存在显着损害的运动性能所测量的旋转棒和楼梯测试。我们的研究结果表明,小鼠光血栓梗死的大小和location.Conclusion:该程序可以提供一个简单的模型,脑梗死的单侧运动皮层病变是高度可重复的。此外,它可以提供一个合适的模型,为研究潜在的神经保护和治疗药物在人类中风。(C)2007爱思唯尔公司All rights reserved.
Background: MCAO has been widely used to produce ischemic brain lesions. The lesions induced by MCAO tend to be variable in size because of the variance in the collateral blood supply found in the mouse brain.Methods: We modified the rat photothrombosis model for use in mice. Male C5713L/6 mice were subjected to focal cerebral ischemia by photothrombosis of cortical microvessels. Cerebral infarction was produced by intraperitoneal injection of rose bengal, a photosensitive dye, and by focal illumination through the skull. Motor impairment was assessed by the accelerating rotarod and staircase tests. The brain was perfusion fixed for histologic determination of infarct volume 4 weeks after stroke.Results: The lesion was located in the frontal and parietal cortex and the underlying white matter was partly affected. A relatively constant infarct volume was achieved I month after photothrombosis. The presence of the photothrombotic lesion significantly impaired the motor performance as measured by the rotarod and staircase tests. Our findings show that photothrombotic infarction in mice is highly reproducible in size and location.Conclusion: This procedure can provide a simple model of cerebral infarction for a unilateral motor cortex lesion. In addition, it can provide a suitable model for the study of potential neuroprotective and therapeutic agents in human stroke. (C) 2007 Elsevier Inc. All rights reserved.