Microglia activation is a critical component of the post-stroke inflammatory response; however, an accumulation of pro-inflammatory activated microglia can have a detrimental effect and lead to cognitive decline. Strokes that affect the basal ganglia can impair behavioural flexibility, an important component of executive function. An association between activated microglia in the white matter tracts and executive dysfunction has been established but not sufficiently evaluated in the context of stroke. Minocycline is a tetracycline derivative shown to effectively inhibit microglia activation. In this study, we used a rat model to investigate the effects of acute post-stroke minocycline treatment on cognitive outcomes and white matter pathology. Stroke was induced in 8-10-month-old male wildtype Fischer 344 rats by injection of endothelin-1 into the right dorsal striatum. Minocycline was administered for 4 days post-stroke prior to testing for behavioural flexibility, learning and memory using an operant conditioning-based set-shifting task and the Morris water maze. Brains were histologically examined at 28 days post-stroke to assess microglia activation, astrogliosis and infarct size. Results indicate a link between white matter activated microgliosis and behavioural outcomes post-stroke suggesting that modifying microglia activation post-stroke could protect the brain and improve cognitive outcomes.

Targeting post-stroke white matter microgliosis using minocycline to prevent cognitive decline in the rat

Western University

Victoria Agapova

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