Jin Kunlin, Sun Yunjuan, Xie Lin, Peel Alyson, Mao Xiao Ou, Batteur Sophie, Greenberg David A
Buck Institute for Age Research, 8001 Redwood Boulevard, Novato, CA 94945, USA.
Mol Cell Neurosci. 2003 Sep;24(1):171-89. doi: 10.1016/s1044-7431(03)00159-3.
Pathological processes, including cerebral ischemia, can enhance neurogenesis in the adult brain, but the fate of the newborn neurons that are produced and their role in brain repair are obscure. To determine if ischemia-induced neuronal proliferation is associated with migration of nascent neurons toward ischemic lesions, we mapped the migration of cells labeled by cell proliferation markers and antibodies against neuronal marker proteins, for up to 2 weeks after a 90-min episode of focal cerebral ischemia caused by occlusion of the middle cerebral artery. Doublecortin-immunoreactive cells in the rostral subventricular zone, but not the dentate gyrus, migrated into the ischemic penumbra of the adjacent striatum and, via the rostral migratory stream and lateral cortical stream, into the penumbra of ischemic cortex. These results indicate that after cerebral ischemia, new neurons are directed toward sites of brain injury, where they might be in a position to participate in brain repair and functional recovery.
包括脑缺血在内的病理过程能够增强成体大脑中的神经发生,但新生神经元的命运及其在脑修复中的作用尚不清楚。为了确定缺血诱导的神经元增殖是否与新生神经元向缺血性损伤部位的迁移有关,我们在大脑中动脉闭塞导致局灶性脑缺血90分钟后长达2周的时间里,绘制了用细胞增殖标记物和抗神经元标记蛋白抗体标记的细胞的迁移图谱。在嘴侧脑室下区而非齿状回中,双皮质素免疫反应性细胞迁移到相邻纹状体的缺血半暗带,并通过嘴侧迁移流和外侧皮质流迁移到缺血皮质的半暗带。这些结果表明,脑缺血后,新神经元被导向脑损伤部位,在那里它们可能参与脑修复和功能恢复。