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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 >Subfield-specific neurovascular remodeling in the entorhino-hippocampal- organotypic slice culture as a response to oxygen-glucose deprivation and excitotoxic cell death
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Subfield-specific neurovascular remodeling in the entorhino-hippocampal- organotypic slice culture as a response to oxygen-glucose deprivation and excitotoxic cell death

机译：内嗅-海马器官型培养中的亚领域特定神经血管重塑，作为对氧-葡萄糖剥夺和兴奋性毒性细胞死亡的反应

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摘要

Transient ischemia causes delayed neurodegeneration in selective brain areas, particularly in the CA1 field of the hippocampus. This is accompanied by neurovascular impairment. It is unknown whether neurodegeneration is the cause or consequence of vascular changes. In an entorhino-hippocampal-organotypic slice culture system with well-preserved blood vessels, we studied the interplay between neurodegeneration and neurovasculature. Short-term oxygen and glucose deprivation (OGD) resulted in upregulation of hypoxic markers and with a delay of 24 to 48 hours in selective nerve cell death in CA1. In parallel, local vessel density decreased as detected by markers of endothelial cells and of the extracellular matrix. Claudin-5, a tight junction protein and marker of the blood-brain barrier was reduced. Preventing neuronal death with tetrodotoxin or 6-cyano-7-nitroquinoxaline-2,3-dione rescued blood vessels, suggesting that vessel loss is not due to OGD per se but a consequence of neuronal death. Induction of excitotoxic neuronal death with AMPA caused widespread neurodegeneration, but vessel reduction was confined to CA1. In dentate gyrus without neuronal loss, vessel density increased. We propose that neuronal stress and death influence maintenance, loss and remodeling of the neurovasculature and that the type of vascular response is in addition determined by local factors within the hippocampus.
机译：短暂性脑缺血会导致选择性大脑区域（尤其是海马CA1区）神经变性的延迟。这伴有神经血管损伤。尚不清楚神经退行性变是血管变化的原因还是后果。在保存完好的血管的内啡肽-海马-有机型切片培养系统中，我们研究了神经变性和神经脉管系统之间的相互作用。短期缺氧和缺糖（OGD）导致缺氧标志物的上调，并导致CA1选择性神经细胞死亡延迟24至48小时。并行地，如通过内皮细胞和细胞外基质的标记所检测的，局部血管密度降低。紧密连接蛋白和血脑屏障标志物Claudin-5减少了。用河豚毒素或6-氰基-7-硝基喹喔啉-2,3-二酮来拯救血管以预防神经元死亡，这表明血管丢失不是由于OGD本身造成的，而是神经元死亡的结果。用AMPA诱发兴奋性毒性神经元死亡会引起广泛的神经变性，但血管减少仅限于CA1。在没有神经元丢失的齿状回中，血管密度增加。我们建议神经元的压力和死亡影响神经脉管系统的维持，丧失和重塑，并且血管反应的类型还由海马内的局部因素决定。

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