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. Author manuscript; available in PMC: 2009 Aug 6.
Published in final edited form as: Dev Neurobiol. 2008 Jul;68(8):1076–1092. doi: 10.1002/dneu.20637

Figure 7. Purkinje cell degeneration in the HDAC4-/- cerebellum.

Figure 7

(A and B) Disrupted lamination pattern in the HDAC4-/- cerebellum. In (A), cell lamination of lobe IX was visualized by DAPI-staining. While the cell sparse molecular layer is clearly delineated in the mutant cerebellum at P3, disruption of the molecular layer is discernible at P4 and extensive at P7. In (B), lamination is visualized using cresyl violet staining of wild-type and HDAC4-/- cerebellum at P7. Circle shows area with disrupted lamination in lobe IX of the HDAC4-/- cerebellum. (SR) Purkinje cell degeneration in the HDAC4-/- cerebellum. In (C), cerebella from HDAC4-/- mice and control littermates were dissected at P3, P4, and P7 and subjected to immunohistochemical analysis with a calbindin antibody. The figure shows the appearance of region containing lobe IX. A normal layer of Purkinje neurons can be observed in lobe IX of the mutant cerebellum at P3. By P4 however, patches lacking Purkinje neurons are visible. Neurodegeneration is more prominent at P7. In (D), calbindin immunohistochemistry was performed on P11 cerebella from HDAC4-/- and mutant cerebellum. Purkinje cell degeneration is also evident in lobe VIII at this stage. (E) Stunted dendritic arborization of Purkinje neurons in the HDAC4-/- cerebellum. Calbindin immunstaining was performed at P7. Figure shows appearance of lobe X.