Figure 7. Impairment of postsynaptic maturation of SMAΔ7 mutants.
A, Postsynaptic acetylcholine receptor (AChR) clusters of mutant sternomastoid muscle are less complex in comparison to those of control NMJs. Bright stripes of fluorescent α-bungarotoxin label, indicative of secondary postsynaptic folds (Marques et al., 2000), are less prominent or lacking in mutant compared to control (insets). Scale bar = 10µm. B, In P12 control sternomastoid, most AChR aggregates have evolved past the plaque stage into an open configuration, while only about 20% have reached this configuration in the mutant. The defects in AChR maturation are less evident in P12 mutant soleus and EDL; however, even control junctions of these muscles are immature at this stage of postnatal development. C, Mutant NMJs are also deficient in junctional folds. Junctional folds appear in parts or all of AChR aggregates in more than 70% of NMJs in P12 control sternomastoid. In contrast, a large majority of NMJs in P12 mutant sternomastoid lack or show patchy, short and/or disoriented stripes of AChR instead. While NMJs of mutant soleus and EDL muscles appear similar to those of mutant sternomastoid, the synapses in the control soleus and EDL muscles are equally immature. A minimum of 20 NMJs each from 3 muscles of each type at P12 were examined; asterisks indicate statistical significance of comparisons (* p<0.05; ** p <0.01)