Functional recovery following
facial nerve injury is poor. Adjacent neuromuscular junctions (NMJs) are "bridged" by terminal Schwann cells and numerous regenerating axonal sprouts. We have recently shown that manual stimulation (MS) restores whisking function and reduces polyinnervation of NMJs. Furthermore, MS requires both
insulin-like growth factor-1 (IGF-1) and
brain-derived neurotrophic factor (
BDNF). Here, we investigated whether
fibroblast growth factor-2 (FGF-2) was also required for the beneficial effects of MS. Following transection and
suture of the facial nerve (facial-facial anastomisis, FFA) in homozygous mice lacking
FGF-2 (
FGF-2(-/-)), vibrissal motor performance and the percentage of poly-innervated NMJ were quantified. In intact
FGF-2(-/-) mice and their wildtype (WT) counterparts, there were no differences in amplitude of vibrissal whisking (about 50°) or in the percentage of polyinnervated NMJ (0%). After 2 months FFA and handling alone (i.e. no MS), the amplitude of vibrissal whisking in WT-mice decreased to 22±3°. In the
FGF-2(-/-) mice, the amplitude was reduced further to 15±4°, that is, function was significantly poorer. Functional deficits were mirrored by increased polyinnervation of NMJ in WT mice (40.33±2.16%) with polyinnervation being increased further in
FGF-2(-/-) mice (50.33±4.33%). However, regardless of the genotype, MS increased vibrissal whisking amplitude (WT: 33.9°±7.7;
FGF-2(-/-): 33.4°±8.1) and concomitantly reduced polyinnervation (WT: 33.9%±7.7;
FGF-2(-/-): 33.4%±8.1) to a similar extent. We conclude that, whereas lack of
FGF-2 leads to poor functional recovery and target reinnervation, MS can nevertheless confer some functional benefit in its absence.