Spatial memory deficits and oxidative stress damage following exposure to lipopolysaccharide in a rodent model of Parkinson's disease

Stimulation of the immune system has been found to enhance, impair, or have no effect on various memory tasks. In the present study, male Wistar rats received saline, lipopolysaccharide (LPS, 250 μg/kg in saline, 7 consecutive days), intranigral 6-hydroxydopamine (6-OHDA, 2 μg/μl saline; 5 μl/site) and intranigral 6-OHDA plus 7 consecutive days of LPS injections and then tested in two cognitive tasks (Y-maze and radial arm-maze). Altered behavioral responses in Y-maze and radial arm-maze tasks were observed in LPS- and LPS + 6-OHDA-treated rats compared to control group. Notably, positive correlations were detected among LPS and LPS + 6-OHDA-treated rats when behavioral deficits were correlated with indicators of oxidative stress. Taken together, we demonstrated that activation of the immune system with LPS administration induced memory impairment and brain oxidative stress, significantly correlated with nigral lesion promoted by 6-OHDA.

► LPS in 6-OHDA-treated group induced spatial memory deficits in Y-maze and radial arm-maze tasks.
► LPS in 6-OHDA-treated group induced memory impairment and oxidative stress with relevance for Parkinson's disease.
► Behavioral deficits within Y-maze and radial arm-maze tasks are significantly correlated to oxidative stress generation.