Fig. 2.

GGF2 induces synaptic loss from innervated neonatal muscles. A–C, Neuromuscular junctions in a normal P9 soleus muscle and (D–F) a P9 soleus muscle exposed to exogenous GGF2 for 5 d. Junctions were triple-labeled with anti-s100 to label SCs (A, D), anti-neurofilament and anti-synaptophysin to label motor axons and their terminals (B, E), and BTx to label AChRs (C, F). At normally innervated junctions, terminal SCs (A) were clustered over nerve terminal arborizations (B) that precisely juxtaposed AChR-rich regions in the postsynaptic muscle membrane (C). At junctions exposed to exogenous GGF2 for 5 d, terminal SCs (D) were poorly organized and had extended processes; nerve terminal arborizations were absent, although motor axons in the intramuscular nerves appeared unperturbed (E). AChRs were no longer clustered into well defined plaques (F). Scale bar, 20 μm.