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Involvement of Nitric Oxide in Spatial Memory Deficits in Status Epilepticus Rats

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Abstract

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.

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Acknowledgements

This work was partly supported by the National Natural Science Foundation of China (30470453, 30640037), Municipal Science Foundation Research of TianJin (06YFJMJC09400).

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Correspondence to Zhuo Yang.

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Liu, Z.W., Zhang, T. & Yang, Z. Involvement of Nitric Oxide in Spatial Memory Deficits in Status Epilepticus Rats. Neurochem Res 32, 1875–1883 (2007). https://doi.org/10.1007/s11064-007-9374-1

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