Muscle-specific deletion of laminin α5 leads to delayed neuromuscular synapse maturation. (A) Laminin α5 protein was undetectable at NMJs by P21 in Lama5M/M mice, but laminin α4 levels were unaltered. Muscle sections were stained with laminin antibodies (green) and Alexa 594–BTX to label AChRs (red). (B) En face views of NMJs in P21 control and Lama5M/M mice stained with antibodies to neurofilaments and SV2 (nerve, green), and Alexa 594–BTX (AChR, red). Motor nerve terminals fully occupied complex AChR clusters in controls. In Lama5M/M muscle, many AChR clusters had a simple morphology and were partially innervated. (C and D) Quantification of topological maturation of AChR clusters (C) and completeness of innervation of AChR clusters (D) in control (open circles) and Lama5M/M (closed squares) sternomastoid muscle. Counts are from two animals per age, >40 NMJs per animal, with the exception of controls at P21 and P40, which are from one animal. (E) Laminin chains present in synaptic BL (adapted from Patton et al., 1997). Bars, 10 μm.
