Involvement of Nitric Oxide in Spatial Memory Deficits in Status Epilepticus Rats
Involvement of Nitric Oxide in Spatial Memory Deficits in Status Epilepticus Rats
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DOI：
10.1007/s11064-007-9374-1
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发表时间：
2007-06
影响因子：
4.4
通讯作者：
Zhaoyang Liu;Tao Zhang;Zhuo Yang
中科院分区：
文献类型：
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作者：
Zhaoyang Liu;Tao Zhang;Zhuo Yang
癫痫持续状态（SE）与认知障碍的显著风险相关，并且已报道SE期间一氧化氮（NO）释放增加。采用Morris水迷宫实验，观察了神经型一氧化氮合酶（nNOS）抑制剂7-硝基吲唑（7-NI）和诱导型一氧化氮合酶（iNOS）抑制剂氨基胍（AG）对大鼠空间学习成绩的影响。7-NI治疗，而不是与AG，改善后SE大鼠的性能，不仅在收购的任务，但也在探测测试。此外，SE诱导的丙二醛（MDA），脂质过氧化的最终产物的水平，显着下降，只有在动物接受7-NI注射。总之，本研究的结果提供了证据表明，NO通路参与了SE后的氧化应激，nNOS/NO通路可能是SE诱导的空间记忆障碍的潜在机制之一。
Status epilepticus (SE) is associated with a significant risk of cognitive impairment, and the increase of nitric oxide (NO) releasing has been reported during SE. We investigated the effects of neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI) and inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), on spatial performance of rats in the Morris water maze. Treatment with 7-NI, but not with AG, improved the performance of rats after SE not only in acquisition of the task but also in probe test. Furthermore, the level of SE-induced malondialdehyde (MDA), end product of lipid peroxidation, was significantly decreased only in animals receiving 7-NI injection. Taken together, the results of the present study provided evidence that the NO pathway contributed to oxidative stress after SE, and nNOS/NO pathway may underlie one of the potential mechanisms contributing to SE-induced spatial memory deficits.