Fine mapping of the spatial relationship between acute ischemia and dendritic structure indicates selective vulnerability of layer V neuron dendritic tufts within single neurons in vivo
Fine mapping of the spatial relationship between acute ischemia and dendritic structure indicates selective vulnerability of layer V neuron dendritic tufts within single neurons in vivo
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DOI：
10.1038/sj.jcbfm.9600428
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发表时间：
2007-06-01
影响因子：
6.3
通讯作者：
Murphy, Timothy H.
中科院分区：
文献类型：
--
作者：
Enright, Lauren E.;Zhang, Shengxiang;Murphy, Timothy H.
我们已经评估了空间之间的关系凝块血管和第V层皮质神经元的结构完整性YFP（黄色荧光蛋白）-H转基因小鼠2至10小时后光血栓中风。幸运的是，由于用于评估体内血流的德克萨斯红葡聚糖被捕获在固定的凝结血管内，因此可以使用组织学在畸形YFP标记的轴突和树突周围精细地绘制缺血区.位于缺血边界的V层神经元的缺血性损伤包含在顶端簇刺状树突结构内，并且没有传播到顶端树突的更近端区域上的棘。树突状细胞损伤的横向传播急剧衰减与缺血边缘的距离（50%减少珠状树突内类似于100 μ m），并随着时间的增加，中风后6小时，但不是此后。轴突损伤也随着时间的推移而增加，但进一步扩展比树突状细胞的损伤，从中风的核心500亩。凋亡和坏死细胞死亡级联激活中风后6小时，然而，只有在300亩的缺血核心。这些数据表明，位于300 μ m以外的缺血区的神经元的轴突和树突电路可以相对自由的损伤或承诺细胞死亡，这表明他们可能是在一个理想的位置，以促进功能恢复。考虑到缺血性损伤可能对涉及表面树突和突出轴突的电路具有更大的影响，可以想象存活的梗死周围神经元可能具有独特的结构和功能特性。
We have evaluated the spatial relationship between clotted vasculature and the structural integrity of layer V cortical neurons in YFP (yellow fluorescent protein)-H transgenic mice 2 to 10 h after photothrombotic stroke. Fortuitously, ischemic zones could be finely mapped about dysmorphic YFP labeled axons and dendrites using histology since texas- red dextran used to assess blood flow in vivo was trapped within fixed clotted vessels. Ischemic damage to layer V neurons located at the border of ischemia was contained within apical tuft spiny dendritic structures and did not propagate to spines on the more proximal region of the apical dendrite. The lateral spread of dendritic damage decayed sharply with distance from the edge of ischemia (50% reduction in beaded dendrites within similar to 100 mu m) and increased with time up to 6 h after stroke but not thereafter. Axonal damage also increased with time but extended further laterally than dendritic damage, up to 500 mu m from the stroke core. Apoptotic and necrotic cell death cascades were activated 6 h after stroke; however, only within 300 mu m of the ischemic core. These data suggest that the axonal and dendritic circuitry of neurons located 300 mu m outside of an ischemic zone can be relatively free of damage or commitment to cell death suggesting that they may be in an ideal position to contribute to functional recovery. Given that ischemic damage may have a larger effect on circuitry involving superficial dendrites and projecting axons, it is conceivable that surviving peri-infarct neurons may have unique structural and functional properties.