Minocycline attenuation of rat corpus callosum abnormality mediated by low-dose lipopolysaccharide-induced microglia activation

Abstract Background Microglia are resident innate immune cells in the brain, and activation of these myeloid results secretion a variety pro-inflammatory molecules, leading to development neurodegenerative disorders. Lipopolysaccharide (LPS) is widely used experimental stimulant microglia activation. We have previously shown that LPS produced evoked detectable functional abnormalities rat corpus callosum (CC) vitro. Here, we further validated effects low-dose LPS-induced resultant white matter abnormality CC an animal model examined its attenuation by anti-inflammatory agent minocycline. Methods Twenty-four SD rats were divided randomly into three groups intra-peritoneally injected daily with saline, LPS, + minocycline, respectively. All animals subject MRI tests 6 days post-injection. The then sacrificed harvest tissues for electrophysiology, western blotting, immunocytochemistry. One-way ANOVA Tukey’s post-test all pair columns was employed statistical analyses. Results Systemic administration microglial as illustrated Iba-1 immunofluorescent staining. observed large number Iba-1-positive hyper-ramified hypertrophic somata or even amoeba like LPS-treated animals, such changes significantly reduced co-administration Electrophysiological recordings axonal compound action potential (CAP) brain slices contained revealed impairment on functionality detected reduction CAP magnitude. Such supported fast transportation evidenced ?-amyloid precursor protein accumulation. These alterations attenuated demonstrating minocycline microglia-mediated interruption integrity function CC. Conclusions