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. Author manuscript; available in PMC: 2014 Jul 3.
Published in final edited form as: Cell. 2013 Jul 3;154(1):118–133. doi: 10.1016/j.cell.2013.05.059

Figure 5. α1A−/−/PC-α1ACTWT transgenic mice have improved phenotype and development of cerebellar cortex compared to α1A−/− mice.

Figure 5

(A and B) The genotype (A) and appearance (B) of α1A−/−/PC-α1ACTWT mice. (C) α1A−/−/PC-α1ACTWT mice had slightly greater body weight compared with α1A−/− mice at age of P14 (*p<0.05). (D) The lifespan of α1A−/−/PC-α1ACTWT mice was significantly improved compared to α1A−/− (*p<0.05). Some pups survived until age of P30 (n = 2, not included in the Figure), while all α1A−/− pups died before P20. (E-H) α1ACT expression improves cerebellar cortex and PC dendrites. Low power images of cerebellar ML (E). PC dendrites are labeled for calbindin-28 kDa (green). The thickness of the ML (F), the relative height of dendritic tree (G), and the density (as defined in Methods) of the PC dendritic tree (H) were reduced in α1A−/− mice and partially corrected in α1A−/−/PC-α1ACTWT mice (100 dendritic trees from 5 mice at each group. Control is set as 1, *p<0.05). (I) Immunolabeling of PFs and PC dendrites using anti-vGlut1 (red) and anti-calbindin (green) antibodies. (J) Immunolabeling of CFs and PC dendrites using anti-vGlut2 (red) and anti-calbindin (green) antibodies. (K and L) Quantitation of CF reach (K) and relative height of dendritic tree (L) (100 CFs, *p<0.05). CF height was measured from the apical pole of PC somata to the tips of vGluT2 labeled CFs. Data are mean ± SEM (see also Figure S5).