Mihály A, Joó F, Szente M
Department of Anatomy, Albert Szent-Györgyi Medical University, Szeged, Hungary.
J Hirnforsch. 1990;31(1):77-86.
The protein transport of the neocortical blood vessels during experimental focal seizures was investigated in adult Wistar rats. The seizure focus was produced by the local application of isosmotic and isohydric 4-aminopyridine solution, while the electrocorticogram was monitored. The protein transport of the vessels was assessed through the histochemical detection of intravenously injected horseradish peroxidase. Serial sections of the whole seizure focus were evaluated in the light microscope, and the areas of protein extravasation were measured planimetrically. Two groups of animals were treated with diphenylhydantoin for 8 days, and the electro-corticographic and seizure experiments were then performed. Three main features of the pathological protein transport were found: 1) the increase in protein permeability was not mediated by a hypertensive crisis during the seizure; 2) the pathologic changes in the neurons and glia always preceded the breakdown of the blood-brain barrier; 3) this breakdown is probably closely related to neuronal hyperactivity, since it was prevented by diphenylhydantoin.
在成年Wistar大鼠中研究了实验性局灶性癫痫发作期间新皮质血管的蛋白质转运。通过局部应用等渗等氢离子的4-氨基吡啶溶液产生癫痫病灶，同时监测脑电图。通过静脉注射辣根过氧化物酶的组织化学检测来评估血管的蛋白质转运。在光学显微镜下评估整个癫痫病灶的连续切片，并通过平面测量法测量蛋白质外渗区域。两组动物用苯妥英治疗8天，然后进行脑电图和癫痫实验。发现了病理性蛋白质转运的三个主要特征：1）癫痫发作期间蛋白质通透性的增加不是由高血压危象介导的；2）神经元和神经胶质细胞的病理变化总是先于血脑屏障的破坏；3）这种破坏可能与神经元的过度活动密切相关，因为它被苯妥英所阻止。
