Platelet CypD–mediated neutrophil recruitment regulates CBF, infarct size, and neurological outcomes following cerebral ischemia-reperfusion. Wild-type C57BL/6J mice (A-F) or CypD^plt−/− mice and littermate controls (CypD^plt+/+) (G-I) were treated with a neutrophil-depleting antibody (anti-Ly6G) or a control antibody (immunoglobulin G [IgG]) 24 hours before the induction of ischemic stroke (eg, tMCAO). (A) The number of circulating neutrophils in IgG- or anti-Ly6G–treated mice, demonstrating that neutrophil depletion with anti-Ly6G was effective. (B) Representative brain sections stained with 2,3,5-triphenyl tetrazolium chloride. Healthy tissue stains red, whereas an absence of staining (white, arrows) indicates infarcted areas. (C) Brain infarct volumes were quantified by planimetric analysis. (D) Neurological outcome was assessed using the Bederson test. (E) Motor function was examined using the grip strength test. (F) CBF was monitored longitudinally in the right MCA territory (the same side as occlusion) before ischemia (baseline), during ischemia, at the start of reperfusion, and at 3 and 24 hours after stroke onset. (G) Circulating neutrophils in CypD^plt−/− and CypD^plt+/+ mice treated with IgG control or an anti-Ly6G antibody to deplete neutrophils. (H) Representative brain sections stained with 2,3,5-triphenyl tetrazolium chloride. Healthy tissue stains red, whereas an absence of staining (white, arrows) indicates infarcted areas. (I) Brain infarct volumes were quantified by planimetric analysis. ns, not significant.