Herrmann Martina, Stern Martin, Vollenweider Florence, Nitsch Cordula
Section of Neuroanatomy, Institute of Anatomy, University of Basel, Pestalozzistr. 20, 4056 Basel, Switzerland.
Exp Brain Res. 2004 Jan;154(2):176-82. doi: 10.1007/s00221-003-1655-6. Epub 2003 Oct 14.
Subthreshold excitotoxic stimuli such as brief cerebral ischemia or chemically induced seizures modulate brain injury resulting from subsequent transient ischemia. Depending on the delay between the two insults, either tolerance or cumulative damage will develop. We were interested whether non-chemically induced inherent epileptic seizures as they occur in Mongolian gerbils have an effect on the outcome of a transient global ischemia, i.e., whether they are an interfering variable in ischemia experiments. Occurrence of spontaneous seizures in adult male gerbils was registered with a video-controlled seizure monitoring system. Bilateral occlusion of common carotid arteries was carried out 2 h or 24 h after the last generalized seizure. After 4 days survival, the extent of ischemia-induced neuronal damage and glial activation were assessed in the hippocampus and striatum. No significant difference in the ischemia induced nerve cell loss was observed in cresyl violet stained sections between the 2-h or 24-h interval gerbils. Neuronal expression of endothelial nitric oxide synthase in CA1 disappeared with neuronal degeneration. Distribution and degree of upregulation of glial fibrillary acidic protein as marker for astrocytes did not differ between the two groups. We concluded that non-chemically induced inherent epileptic seizures neither protect the gerbil brain from injury nor augment the degree of damage resulting from transient forebrain ischemia. Thus, inherent epileptic seizures do not influence the outcome of the insult, making the gerbil a reliable model for studies on transient brain ischemia.
亚阈值兴奋性毒性刺激，如短暂性脑缺血或化学诱导的癫痫发作，可调节随后短暂性缺血所致的脑损伤。根据两次损伤之间的间隔时间，会产生耐受性或累积性损伤。我们感兴趣的是，蒙古沙鼠中发生的非化学诱导的固有癫痫发作是否会对短暂性全脑缺血的结果产生影响，即它们是否是缺血实验中的一个干扰变量。使用视频控制的癫痫监测系统记录成年雄性沙鼠的自发性癫痫发作情况。在最后一次全身性癫痫发作后2小时或24小时，进行双侧颈总动脉闭塞。存活4天后，评估海马体和纹状体中缺血诱导的神经元损伤和胶质细胞激活的程度。在甲酚紫染色切片中，2小时或24小时间隔的沙鼠之间，缺血诱导的神经细胞丢失没有显著差异。CA1区内皮型一氧化氮合酶的神经元表达随着神经元变性而消失。两组之间作为星形胶质细胞标志物的胶质纤维酸性蛋白的上调分布和程度没有差异。我们得出结论，非化学诱导的固有癫痫发作既不能保护沙鼠大脑免受损伤，也不会增加短暂性前脑缺血所致的损伤程度。因此，固有癫痫发作不会影响损伤结果，这使得沙鼠成为研究短暂性脑缺血的可靠模型。
