Figure 2.

Myotendinous and neuromuscular junctions are maintained in α7BX2 transgenic mice. A: Structure of the myotendinous junctions of gastrocnemius muscle of 5-week-old wild-type, mdx, mdx/utr^−/−, and α7BX2-mdx/utr^−/− mice. The sarcolemma of the myotendinous junction in wild-type and mdx mice is highly folded (arrows), increasing the contact between muscle and tendon. In contrast, the sarcolemma of the myotendinous junction in the severely dystrophic mdx/utr^−/− mice exhibits little folding. Enhanced expression of the α7BX2 transgene in mdx/utr^−/− mice results in maintenance of sarcolemmal folding similar to that seen in wild-type and mdx mice. B: Quantitation of sarcolemmal folds at the myotendinous junction reveals a slight reduction in folding in mdx mice compared to wild-type. In contrast, a sixfold reduction in sarcolemmal folds at the myotendinous junction, was scored in mdx/utr^−/− mice. Expression of the α7BX2 transgene maintains near normal folding of the sarcolemma in mdx/utr^−/− mice. C: A mild reduction in postsynaptic folding of the neuromuscular junctions of sternomastoid muscles is observed in mdx mice compared to wild-type animals whereas a major reduction in junctional folds occurs in mdx/utr^−/− mice.36 Expression of the α7BX2 transgene in mdx/utr^−/− mice results in a maintenance of postsynaptic folding comparable to that observed in mdx mice. Folds at the myotendinous and neuromuscular junctions were counted for at least 10 junctions per animal (n = 3 mice per genotype). The standard errors of the mean values for each animal within each group are indicated. P < 0.05 for comparisons of transgenic and nontransgenic mice.