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首页> 外文期刊>The European Journal of Neuroscience >A spatiotemporal study of gliosis in relation to depth electrode tracks in drug-resistant epilepsy
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A spatiotemporal study of gliosis in relation to depth electrode tracks in drug-resistant epilepsy

机译：胶质瘤与耐药性癫痫的深度电极轨迹相关的时空研究

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Key questions remain regarding the processes governing gliogenesis following central nervous system injury that are critical to understanding both beneficial brain repair mechanisms and any long-term detrimental effects, including increased risk of seizures. We have used cortical injury produced by intracranial electrodes (ICEs) to study the time-course and localization of gliosis and gliogenesis in surgically resected human brain tissue. Seventeen cases with ICE injuries of 4-301 days age were selected. Double-labelled immunolabelling using a proliferative cell marker (MCM2), markers of fate-specific transcriptional factors (PAX6, SOX2), a microglial marker (IBA1) and glial markers (nestin, GFAP) was quantified in three regions: zone 1 (immediate vicinity: 0-350 μm), zone 2 (350-700 μm) and zone 3 (remote ≥2000 μm) in relation to the ICE injury site. Microglial/macrophage cell densities peaked at 28-30 days post-injury (dpi) with a significant decline in proliferating microglia with dpi in all zones. Nestin-expressing cells (NECs) were concentrated in zones 1 and 2, showed the highest regenerative capacity (MCM2 and PAX6 co-expression) and were intimately associated with capillaries within the organizing injury cavity. There was a significant decline in nestin/MCM2 co-expressing cells with dpi in zones 1 and 2. Nestin-positive fibres remained in the chronic scar, and NECs with neuronal morphology were noted in older injuries. GFAP-expressing glia were more evenly distributed between zones, with no significant decline in density or proliferative capacity with dpi. Colocalization between nestin and GFAP in zone 1 glial cells decreased with increasing dpi. In conclusion, NECs at acute injury sites are a proliferative, transient cell population with capacity for maturation into astrocytes with possible neuronal differentiation observed in older injuries.
机译：关于控制中枢神经系统损伤后神经胶质发生的过程，仍然存在关键问题，这对于理解有益的大脑修复机制和任何长期有害影响（包括增加癫痫发作的风险）都是至关重要的。我们已使用颅内电极（ICE）产生的皮质损伤来研究手术切除的人脑组织中神经胶质形成和神经胶质形成的时程和定位。选择了17例4-301日龄的ICE损伤。在三个区域中对使用增生细胞标记物（MCM2），命运特异性转录因子标记物（PAX6，SOX2），小胶质标记物（IBA1）和神经胶质标记物（nestin，GFAP）进行的双标记免疫标记进行了定量：三个区域：1区（立即区域：相对于ICE损伤部位的0-350μm），2区（350-700μm）和3区（远程≥2000μm）。小胶质细胞/巨噬细胞的细胞密度在损伤后（dpi）的28-30天达到峰值，在所有区域中，随着dpi的增加，小胶质细胞的增殖显着下降。巢蛋白表达细胞（NEC）集中在区域1和2中，显示出最高的再生能力（MCM2和PAX6共表达），并且与组织损伤腔内的毛细血管紧密相关。在区域1和区域2中，巢蛋白/ MCM2共表达细胞显着下降，且dpi下降。巢蛋白阳性纤维保留在慢性疤痕中，老年损伤中发现神经元形态的NEC。表达GFAP的胶质细胞在区域之间分布更均匀，且密度或dpi的增殖能力没有明显下降。 1区神经胶质细胞中Nestin和GFAP之间的共定位随dpi的增加而降低。总之，急性损伤部位的NEC是一种增殖性瞬时细胞群，具有成熟为星形胶质细胞的能力，在老年损伤中可能会出现神经元分化。

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