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

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.

Low‐intensity physical training recovers object recognition memory impairment in rats after early‐life induced Status epilepticus

“…2). These data indicate that prolonged seizures early in life can cause long-standing cognitive impairments in object recognition memory, which corroborates with another work that observed that SE can induce memory impairments in animals subjected to the Morris water maze and inhibitory avoidance tasks (de Oliveira et al, 2008;Kubová et al, 2004;Liu et al, 2007). SE induces massive neurodegeneration in several brain regions, including the hippocampus and perirhinal cortex (Wang et al, 2008).…”

Inducible nitric oxide inhibitor aminoguanidine, ameliorates deleterious effects of lipopolysaccharide on memory and long term potentiation in rat

“…These discrepancies might be due to a high dose which was used for a long period in our previous study. Additionally, in another study AG did not affect learning and memory in spatial task in rats with status epilepticus [59]. In contrast, treatment with AG also ameliorated hypoxia-induced retrograde memory impairment in Balb/ c mice [60].…”

Serum Nitrosative Stress Levels Are Increased in Alzheimer Disease but Not in Vascular Dementia

“…The study of Cankurtaran et al 19 indicated that independent correlates are female sex, advanced age, depression, and intake of vitamin supplements for AD; and depression and LDL-C for VaD. Some authors indicate that there is a relationship between cognitive status and NO levels, 26 whereas others have not found any. In the nervous system, NO seems to have both neurotoxic and neuroprotective effects, and it may have a role in the pathogenesis of stroke and other neurodegenerative disease, including AD associated with the activation of glial cells and the production of proinflammatory cytokines where the brain microvessels produce high level of NO.…”