A Single Lipopolysaccharide (LPS) Injection to the Rat Brain Induces Neuroinflammation Two Months After Treatment
Kaptur, Kendall G.
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The topic of neuroinflammation and its effects on the brain pathology and function has motivated some relevant research questions. Researchers have found that the key mediators in the inflammatory responses in the brain are known as microglia. The negative effects of microglia have been studied, as well as instigators that elicit this inflammatory response. Microglial activation and neuroinflammation are key factors in the pathogenesis related to numerous neurodegenerative diseases. Identifying the responsible stimuli and mechanisms that cause progressive microglial activation and neuron damage may be crucial for understanding the etiology and pathology of neurodegenerative diseases. One known instigator of neuroinflammation is lipopolysaccharide (LPS), an endotoxin from gram-negative bacteria. The aim of this study was to see if a single LPS injection can induce neuroinflammation and microglial activation two months after treatment, as well as if a single LPS injection could produce any measurable behavioral/cognitive deficits such as an increase in impulsivity. Immunohistochemical staining techniques were used to view microglial activation in the brain tissue, and a behavioral assay involving inter-temporal choice trials was implemented to measure differences in rat behavior and cognition. The results show that a single LPS dose two months after treatment is sufficient to induce neuroinflammation and microglial activation. However, there was no significant difference in rat behavior/impulsivity between groups. Further research using this behavior model with a larger sample size would allow for a better understanding if LPS can produce significant changes in behavior. Additionally, investigations about microglia quantity in specific brain regions could be beneficial to gain a better understanding of the effects LPS has on all areas and structures of the brain. Forwarding research in both of these models could possibly provide better understandings of neurodegenerative diseases and treatments.