Effects of Peripheral Lipopolysaccharide Administration on Spatial Memory and Passive Avoidance Learning in Rats

Neuro-inflammation, is one of an early events in the pathogenesis of Alzheimer’s disease (AD) as well as loss of synapses, microglial activation, and accumulation of amyloid beta (Aβ). Stimulating the immune responses in the brain and releasing inflammatory mediators cause to generate oxidative stress agents. Lipopolysaccharide (LPS), a toxic part of gram negative bacterial cells which are found inthe outer membrane of these cells, has been classically proposed as trigger for immune system to release the pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6. The purpose of this study was to assess, the effects of LPS on memory impairment in rats. Then, oxidativestress biomarkers in both cortex and hippocampal formation were evaluated. Materials and Methods: The experimental animals were described as: (1) control, (2) LPS. In order to measure the biochemical markers, the brain tissues were removed. (n=10 in each group).Results: Time spent in target quadrant in the Morris water maze task and the delay time to enter the dark part in the passive avoidance learning task were significantly shorter in LPS treated group compared to the control group. The concentration of Malondialdehyde (MDA),in the cortex and hippocampus of the LPS treated rats significantly increased compared to the control group. The total content of the thiol group, the activities of catalase (CAT) and superoxide dismutase (SOD) in cortical and hippocampal tissues of LPS treated rats decreased regarding to the control group. Conclusion: These results indicated that LPS could disturb the brain’s immune system towards memory destruction by increasing oxidative stress biomarkers.