Research reportIntranigral lipopolysaccharide administration induced behavioral deficits and oxidative stress damage in laboratory rats: Relevance for Parkinson's disease

- Intranigral LPS injection induced spatial memory deficits.
- Intranigral LPS injection induced oxidative stress in temporal cortex.
- Behavioral deficits within Y-maze are correlated to oxidative stress generation.

In the present study, we examined whether oxidative stress in the hippocampus contributes to memory deficits induced by unilateral injections of two different doses of lipopolysaccharide (3 μg/kg and 10 μg/kg) into the substantia nigra of adult male Wistar rats. Pergolide-induced rotational behavior test was employed to validate unilateral damage to the dopamine nigrostriatal neurons. Lipopolysaccharide-induced memory impairments were observed, as measured by the Y-maze and radial arm-maze tasks. Decreased activities of superoxide dismutase and glutathione peroxidase were observed in the rat hippocampal homogenates of lipopolysaccharide-treated animals as compared with control. Production of malondialdehyde (lipid peroxidation) significantly increased in the rat hippocampal homogenates of lipopolysaccharide-treated animals as compared with control, as a consequence of impaired antioxidant enzymes activities. Additionally, only within Y-maze, significant correlations between behavioral deficits and indicators of oxidative stress were found.However, further studies are necessary in order to elucidate the effects of intranigral lipopolysaccharide administration on memory performance and oxidative stress status and also the possible correlation that might exist between these aspects.