To impair microglial function, mice received a daily oral administration by gavage of the CSF1R inhibitor GW2580 [12 (link)] (75 mg/kg body weight in a volume of 0.2 mL) (#S8042, Selleckchem) for 4 days, which is a dosing regimen that does not challenge microglial survival [54 (link)]. Treatment controls received the same volume of the vehicle (0.5% hydroxypropylcellulose, 0.1% Tween-80). Treatment started 2 h prior to induction of ischemia, it was randomly allocated, and was administered in a blinded fashion.
For microglia depletion, mice received the CSF1R inhibitor PLX5622 (Plexxikon) following previously reported protocols [15 (link), 33 (link), 69 (link)]. The inhibitor was mixed into AIN-76A standard chow at 1200 ppm (Brogaarden, Denmark). Mice (8-week-old) received the diet ad libitum for 3 weeks prior to induction of ischemia and the diet was maintained until the mice were killed. Treatment controls received AIN-76A diet for the same period of time. Both diets were given in parallel in groups of five animals per cage.
For microglia depletion, mice received the CSF1R inhibitor PLX5622 (Plexxikon) following previously reported protocols [15 (link), 33 (link), 69 (link)]. The inhibitor was mixed into AIN-76A standard chow at 1200 ppm (Brogaarden, Denmark). Mice (8-week-old) received the diet ad libitum for 3 weeks prior to induction of ischemia and the diet was maintained until the mice were killed. Treatment controls received AIN-76A diet for the same period of time. Both diets were given in parallel in groups of five animals per cage.
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