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与局灶性中风相邻的功能性皮质亚区内的组织微环境。

Tissue microenvironments within functional cortical subdivisions adjacent to focal stroke.

作者信息

Katsman Diana, Zheng Jian, Spinelli Kateri, Carmichael S Thomas

机构信息

Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.

出版信息

J Cereb Blood Flow Metab. 2003 Sep;23(9):997-1009. doi: 10.1097/01.WCB.0000084252.20114.BE.

DOI:10.1097/01.WCB.0000084252.20114.BE
PMID:12973016
Abstract

Stroke produces a region of complete cell death and areas of partial damage, injury, and gliosis. The spatial relationship of these regions of damage to the infarct core and within spared neuronal circuits has not been identified. A model of cortical stroke was developed within functional subsets of the somatosensory cortex. Infarct size, regions of apoptosis, oxidative DNA damage, heat shock protein induction, and subtypes of reactive gliosis were precisely mapped with the somatosensory body map, quantified, and interrelated. Three tissue microenvironments were recognized: zones of partial ischemic damage, heat shock protein induction, and distributed gliosis. These three zones involved progressively more distant cortical regions, each larger than the infarct core. The zone of partial ischemic damage represents an overlap region of apoptotic cell death, oxidative DNA damage, loss of synaptic connections, and local reactive gliosis. The zone of distributed gliosis occupies distinct functional areas of the somatosensory cortex. The tissue reorganization induced by stroke is much larger than the stroke site itself. Adjacent tissue microenvironments are sites of distinct reactive cellular signaling and may serve as a link between the processes of acute cell death and delayed neuronal plasticity after focal stroke.

摘要

中风会产生一个完全细胞死亡区域以及部分损伤、伤害和胶质增生区域。这些损伤区域与梗死核心以及未受损神经回路之间的空间关系尚未明确。在体感皮层的功能亚组内建立了皮质中风模型。梗死大小、凋亡区域、氧化性DNA损伤、热休克蛋白诱导以及反应性胶质增生的亚型均通过体感人体图谱进行了精确绘制、量化并相互关联。识别出三种组织微环境:部分缺血损伤区、热休克蛋白诱导区和弥漫性胶质增生区。这三个区域涉及逐渐更远的皮质区域,每个区域都比梗死核心大。部分缺血损伤区代表凋亡细胞死亡、氧化性DNA损伤、突触连接丧失和局部反应性胶质增生的重叠区域。弥漫性胶质增生区占据体感皮层的不同功能区域。中风诱导的组织重组比中风部位本身大得多。相邻的组织微环境是不同反应性细胞信号传导的部位,可能是局灶性中风后急性细胞死亡和延迟神经元可塑性过程之间的联系。

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