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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >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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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.

机译:急性缺血和树突结构之间的空间关系的精细映射表明体内单个神经元内的V层神经元树突簇的选择性脆弱性。

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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 approximately 100 microm) 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 microm from the stroke core. Apoptotic and necrotic cell death cascades were activated 6 h after stroke; however, only within 300 microm of the ischemic core. These data suggest that the axonal and dendritic circuitry of neurons located 300 microm 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.
机译:我们已经评估了血栓形成性卒中后2至10小时,YFP(黄色荧光蛋白)-H转基因小鼠中凝结的脉管系统与V层皮质神经元的结构完整性之间的空间关系。幸运的是,可以使用组织学方法将异形YFP标记的轴突和树突细化到局部缺血区域,因为用于评估体内血流的德州红葡聚糖被困在固定的凝结血管中。对位于缺血边界的V层神经元的缺血性损伤被包含在顶端簇状棘状树突结构内,并且没有传播到顶端树突的更近端区域上的棘。树突损伤的侧向扩散随着距缺血边缘的距离而急剧衰减(大约100微米内的珠状树突减少了50%),并在中风后直至6 h随时间增加,但此后没有增加。轴突损伤也随时间增加,但比树突状损伤更向侧面延伸,距中风核心最远为500微米。中风后6小时激活了凋亡和坏死细胞死亡级联反应。但是,仅在缺血核心的300微米之内。这些数据表明,位于缺血区以外300微米处的神经元的轴突和树突状回路可能相对没有损伤或对细胞死亡的承诺,表明它们可能处于有助于功能恢复的理想位置。考虑到缺血性损伤可能对涉及浅表树突和突出的轴突的电路有更大的影响,可以想象存活的梗塞周围神经元可能具有独特的结构和功能特性。

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