Dynamic secondary degeneration in the spinal cord and ventral root after a focal cerebral infarction among hypertensive rats.
Dynamic secondary degeneration in the spinal cord and ventral root after a focal cerebral infarction among hypertensive rats.
复制标题
高血压大鼠局灶性脑梗死后脊髓和腹侧根的动态继发性变性。
DOI：
10.1038/srep22655
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发表时间：
2016-03-07
影响因子：
4.6
通讯作者：
Zeng J
中科院分区：
文献类型：
--
作者：
Dang G;Chen X;Chen Y;Zhao Y;Ouyang F;Zeng J
脑梗塞可对非脑缺血区造成继发性损害。然而，这种现象是否会出现在大脑以外的中枢神经系统区域仍不清楚。在这里，我们研究了缺血性中风后脊髓和前根的病理变化。所有大鼠在MCAO后都表现出明显的神经功能障碍，并逐渐改善，但在12周时仍可检测到。大脑中动脉闭塞后1周，对侧颈腰椎膨大的皮质脊髓束(CST)神经元细丝和前角神经元明显减少。这些下降保持稳定，直到12周，伴随着腹角神经胶质细胞活性的逐渐增加。大脑中动脉阻塞后1周，对侧颈和腰椎前根轴突变性和结构紊乱明显；这些变化随着时间的推移自发减弱，但在12周仍可观察到异常。MCAO后12周，对侧大脑中隔核神经纤维数量和对侧腹角神经元数量与神经功能评分呈正相关。此外，健侧CST和前角GFAP+细胞密度与神经功能评分呈负相关。我们的结果表明，脑梗塞可引起颈、腰段脊髓以及突起的前根的继发性变性，这可能阻碍中风后的功能恢复。
Cerebral infarction can cause secondary damage to nonischemic brain regions. However, whether this phenomenon will appear in central nervous system regions outside the brain remains unclear. Here we investigated pathological changes in the spinal cord and ventral root after ischemic stroke. All rats exhibited apparent neurological deficits post-MCAO, which improved gradually but could still be detected 12-weeks. Neuronal filaments in the corticospinal tract (CST) and neurons in the ventral horn were significantly declined in the contralateral cervical and lumbar enlargement 1-week post-MCAO. These decreases remained stable until 12-weeks, accompanied by progressively increased glial activation in the ventral horn. Axonal degeneration and structural derangement were evident in the contralateral cervical and lumbar ventral root 1-week post-MCAO; these changes spontaneously attenuated over time, but abnormalities could still be observed 12-weeks. The number of neural fibers in the contralateral CST and neurons in the contralateral ventral horn were positively correlated with neurological scores 12-weeks post-MCAO. Additionally, GFAP+cell density in the contralateral CST and ventral horn was negatively correlated with neurological scores. Our results suggest that cerebral infarction can elicit secondary degeneration in the cervical and lumbar spinal cord, as well as the projecting ventral root, which may hamper functional recovery after stroke.