Induction of thrombocytopenia in neonates results in cerebellar hemorrhage. (A) (i) Image highlighting the facial vein of a P1 mouse used to deliver anti-GP1bα and IgG control antibodies. (ii) Representative flow cytometry plots of P1 peripheral blood stained with markers of erythrocytes (TER119) and platelets (CD41). (iii) Quantification of circulating platelets at 6 hours (IgG n = 8, GP1Bα n = 8) and 48 hours (IgG n = 4, GP1Bα n = 4) posttreatment. (B) Representative image of a P1 neonate 48 hours after treatment with anti-GP1bα (n = 7 embryos). Yellow arrows indicate sites of hemorrhage. (C) (i-iii) Representative images of brains 6 hours (IgG n = 8, GP1Bα n = 8) and 48 hours (IgG n = 4, GP1Bα n = 4) posttreatment. Yellow arrows indicate sites of cortical hemorrhage; the blue arrow highlights cerebellar hemorrhage (scale bars, 1 mm). (D) Coronal sections of cerebellum 48 hours posttreatment (bars, 1 mm). (E) Frequency of cerebellar hemorrhage in mice treated at E16.5 (IgG n = 10, GP1Bα n = 16), E17.5 (IgG n = 10, GP1Bα n = 12), or P1 (IgG n = 4, GP1Bα n = 7). (F) Summary of changes in ICH location during embryogenesis. ICHs in the ganglionic eminence, cortex, and cerebellum occur sequentially during development in a thrombocytopenic context.