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FGF receptor 2 is involved in the formation of the neuromuscular junction (NMJ), but its  in vivo  ligand remains to be determined. Laser capture microdissection of the mouse spinal motor neurons (SMNs) revealed that  Fgf18  mRNA is highly expressed in SMNs in adults. Expression of  Fgf18  mRNA was the highest in the spinal cord at embryonic day (E) 15.5, which gradually decreased to postnatal day 7. FGF18 protein was localized at the NMJs of the tibialis anterior muscle at E18.5 and in adults.  Fgf18 −/− mice at E18.5 showed decreased expressions of the NMJ-specific  Chrne  and  Colq  genes in the diaphragm. In  Fgf18 −/− diaphragms, the synaptophysin-positive areas at the nerve terminals and the acetylcholine receptor (AChR)-positive areas at the motor endplates were both approximately one-third of those in wild-type embryos.  Fgf18 −/− diaphragms ultrastructurally showed abnormal aggregation of multiple nerve terminals making a gigantic presynapse with sparse synaptic vesicles, and simplified motor endplates. In  Fgf18 −/− diaphragms, miniature endplate potentials were low in amplitude with markedly reduced frequency. In C2C12 myotubes, FGF18 enhanced AChR clustering, which was blocked by inhibiting FGFRs or MEK1. We propose that FGF18 plays a pivotal role in AChR clustering and NMJ formation in mouse embryogenesis.

Lack of Fgf18 causes abnormal clustering of motor nerve terminals at the neuromuscular junction with reduced acetylcholine receptor clusters