Irradiation attenuates neurogenesis and exacerbates ischemia-induced deficits
Irradiation attenuates neurogenesis and exacerbates ischemia-induced deficits
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DOI：
10.1002/ana.10853
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发表时间：
2004-03-01
影响因子：
11.2
通讯作者：
Liu, JL
中科院分区：
文献类型：
--
作者：
Raber, J;Fan, Y;Liu, JL
脑缺血后增加的神经发生表明中风后的功能恢复可能部分归因于神经再生。在这项研究中，我们研究了沙土鼠全脑缺血后神经发生在行为表现中的作用。采用电离辐射抑制神经再生，2周后采用双侧颈总动脉闭塞法造成全脑缺血。闭塞后一个月，对动物进行行为测试。在行为测试时，单独照射减少了神经发生，但没有改变血管或树突的形态。辐照、局部缺血或联合治疗均未损害转子杆性能或改变旷场活动。与仅接受局部缺血、放射或未接受治疗的沙鼠相比，接受放射和局部缺血的沙鼠在水迷宫任务中表现出受损的表现。在神经发生减少的条件下，全脑缺血后的这些损伤支持新细胞的产生在介导功能恢复中的作用。
Increased neurogenesis after cerebral ischemia suggests that functional recovery after stroke may be attributed, in part, to neural regeneration. In this study, we investigated the role of neurogenesis in the behavioral performance of gerbils after cerebral global ischemia. We used ionizing radiation to decrease neural regeneration, and 2 weeks later cerebral global ischemia was induced by bilateral common carotid artery occlusion. One month after the occlusion, the animals were behaviorally tested. Irradiation alone reduced neurogenesis but did not change vascular or dendritic morphology at the time of behavioral testing. Neither did irradiation, ischemia, or combined treatment impair rotor-rod performance or alter open-field activity. Gerbils subjected to both irradiation and ischemia demonstrated impaired performance in the water-maze task, compared with those that received only ischemia, radiation, or no treatment. These impairments after cerebral global ischemia under conditions of reduced neurogenesis support a role for the production of new cells in mediating functional recovery.