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Files in this Data Supplement:
Fig. S1. Neural and vascular pathologies in neonatal and adult β8−/− mice. (A) Images of brains dissected from newborn (P0) wild-type and β8−/− mice generated on an ICR/CD-1 background. Note the obvious intracerebral hemorrhage in the β8−/− mutants; this phenotype occurs with similar severity in all newborn animals that have been analyzed. (B) Hematoxylin and Eosin (H&E) stained sagittal sections from P60 wild-type and β8−/− mice. Note the absence of intracerebral hemorrhage in adult mutants, although hydrocephalus (asterisk) is obvious in most mutants. The lower panel shows a particularly severe example of hydrocephalus. (C,D) H&E staining of coronal brain sections from P60 wild-type (C) and β8−/− (D) mice reveals absence of the corpus callosum (cc) in mutant animals (arrows in D). (E, F) H&E staining of coronal brain sections from P60 wild-type (E) and β8−/− (F) mice reveals abnormal hippocampal dentate gyrus cytoarchitecture in β8−/− animals. Note the abnormal thickness of the β8−/− hilus (h). (G,H) Silver staining of coronal sections through the brains of wild-type (G) and mutant (H) mice reveals abnormal dendritic projections in the CA3 layers of the hippocampal dentate gyrus of β8−/− animals (arrows in H).
Fig. S2. Analysis of cerebellar cytoarchitecture in adult β8−/− mice. (A-D) Sagittal H&E-stained sections from the cerebellums of P60 wild-type (A,C) and β8−/− (B,D) mice. Note the apparently normal Purkinje cell organization in the wild-type and β8−/− brains (arrows in C,D). Cerebellar white matter degeneration has not been detected in adult β8−/− mice. C and D are higher magnification images of boxed areas in A and B. GCL, granular cell layer; WM, white matter.
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