GM1单唾液神经节苷预处理可预防soman诱导的癫痫相关脑损伤。

G P Ballough, F J Cann, C D Smith, J S Forster, C E Kling, M G Filbert
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引用次数: 19

摘要

本研究探讨了GM1单唾液神经节苷预处理对梭曼诱发癫痫发作引起的脑损伤的影响。雄性Sprague-Dawley大鼠通过植入脑室内的永久插管连接的渗透性微型泵注入GM1,并在GM1输注开始后第4天注入soman(83微克/千克,即1.25 × LD50)。通过留置皮质电极监测皮质电图记录。给药27小时后,麻醉大鼠经心肌灌注缓冲多聚甲醛安乐死。对脑组织进行苏木精和伊红(H&E)、甲酰紫(CV)、乙酰胆碱酯酶(AChE)组织化学以及胶质纤维酸性蛋白(GFAP)和微管相关蛋白2 (MAP2)免疫组织化学处理。所有未注射GM1的索曼挑战大鼠(n = 14)均出现癫痫持续状态(SE)。
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GM1 monosialoganglioside pretreatment protects against soman-induced seizure-related brain damage.

The effects of GM1 monosialoganglioside pretreatment on brain damage resulting from soman-induced seizure activity were examined in this study. Male Sprague-Dawley rats were infused with GM1 via an osmotic minipump connected through a permanent cannula implanted intracerebroventricularly and challenged with soman (83 micrograms/kg, i.e., 1.25 x LD50) 4 d after initiation of GM1 infusion. Electrocorticographic recordings were monitored via indwelling cortical electrodes. Twenty-seven hours after soman administration, anesthetized rats were euthanized via transcardial perfusion with buffered paraformaldehyde. Brains were processed for hematoxylin and eosin (H&E), cresyl violet (CV), and acetylcholinesterase (AChE) histochemistry, and glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP2) immunohistochemistry. All soman-challenged rats not infused with GM1 (n = 14) developed status epilepticus (SE).

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