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首页> 外文期刊>The European Journal of Neuroscience >Cerebral oligaemia episode triggers free radical formation and late cognitive deficiencies.
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Cerebral oligaemia episode triggers free radical formation and late cognitive deficiencies.

机译:脑低血糖发作可引发自由基形成和晚期认知缺陷。

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Sixty minutes of cerebral oligaemic hypoxia, induced by bilateral clamping of the carotid arteries (BCCA) in pentobarbital-anaesthetized normotensive rats, induces a late progressive cognitive decline when compared with sham-operated controls. Analysis at BCCA of hippocampal metabolism using microdialysis showed increased release of glutamate, aspartate and gamma-aminobutyric acid, followed by a progressive rise in the formation of hydroxyl free radicals measured as 2,3-dihydroxybenzoic acid (2,3-DHBA), their reaction product with salicylate, though only in the re-perfusion phase. In the striatum increased dopamine release occurred during BCCA, whereas glutamate and aspartate showed an increase only during the late re-perfusion phase. gamma-Aminobutyric acid (GABA) concentration increased during BCCA and early re-perfusion. An increase in 2,3-DHBA was seen during BCCA, and persisted over 2 h of re-perfusion. Six and 13 months after surgery, though not as early as 3 months, BCCA-treated rats perform worse than sham-operated controls in a water-maze, where decreased swimming speed reveals striatal dysfunction, while hippocampal dysfunction manifested as diminished spatial bias. These results show that cerebral oligaemia, similarly to cerebral ischaemia, leads to increased extracellular dopamine, aspartate and glutamate, and the production of hydroxyl radicals in structures associated with learning and memory processes. Unlike cerebral ischaemia, in cerebral oligaemia the appearance of spatial memory deficits is delayed.
机译:与假手术对照组相比,戊巴比妥麻醉的血压正常大鼠的颈动脉双侧钳夹(BCCA)诱发了60分钟的大脑低氧血症性缺氧。使用微透析在BCCA进行的海马代谢分析表明,谷氨酸,天冬氨酸和γ-氨基丁酸的释放增加,随后以2,3-二羟基苯甲酸(2,3-DHBA)的形式出现的羟基自由基形成逐渐增加。与水杨酸酯的反应产物,尽管仅在再灌注阶段。在BCCA期间,纹状体中多巴胺的释放增加,而谷氨酸和天门冬氨酸仅在再灌注后期才显示出增加。在BCCA和早期再灌注期间,γ-氨基丁酸(GABA)浓度增加。在BCCA期间观察到2,3-DHBA的增加,并在2小时的再灌注过程中持续存在。手术后六个月和十三个月,虽然不是最早三个月,但在水迷宫中,用BCCA治疗的大鼠的表现要比假手术的对照组差,后者的游泳速度降低显示出纹状体功能障碍,而海马功能障碍则表现为空间偏倚减少。这些结果表明,与脑缺血相似,脑性低血症会导致细胞外多巴胺,天冬氨酸和谷氨酸增加,并在与学习和记忆过程有关的结构中产生羟基自由基。与脑缺血不同,在脑低血糖症中,空间记忆缺陷的出现会延迟。

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