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. Author manuscript; available in PMC: 2008 Mar 1.
Published in final edited form as: Neuromuscul Disord. 2007 Feb 14;17(3):209–220. doi: 10.1016/j.nmd.2006.12.004

Figure 1.

Figure 1

Overexpression of CT carbohydrate inhibits muscle pathology up to 18 months of age in Galgt2 transgenic mdx mice.

(A) Central nuclei were quantitated in skeletal muscles taken from wild type (Wt), Galgt2 transgenic (CT), mdx, and Galgt2-transgenic mdx (mdx/CT) mice at the indicated ages. Skeletal muscles analyzed (from left to right) were gastrocnemius, trapezius, diaphragm, triceps, quadriceps, tibialis anterior, and gluteus maximus. CT muscles began to develop some central nuclei at 18 months of age, as did mdx/CT muscles, however, the percentage of myofibers with central nuclei in mdx/CT animals was still significantly lower than mdx littermates for all muscles (P<0.001 for all) at 12 and 18 months of age. Errors are SEM for n=250 fibers per muscle for 3-4 animals per condition. (B) Hematoxylin and eosin staining of muscles at 18 months of age showed that CT and mdx/CT myofibers were significantly smaller than wild type (gastrocnemius is shown) and relatively free from muscle damage. Bar is 50μm. (C) Rhodamine-α-bungarotoxin of Wt and CT muscles in cross-section (larger panels) or in whole mount (smaller panels) shows aberrant neuromuscular junctions in CT muscles as compared to wild type at 18 months of age as well. Bar is 25μm (larger panels) or 12.5μm (smaller panels).