Comparison of trophic factors' expression between paralyzed and recovering muscles after facial nerve injury. A quantitative analysis in time course

Immunohistochemical Detection of Motor Endplates in the Long-Term Denervated Muscle

“…There is growing evidence suggesting that some neurotrophic factors such as nerve growth factor, basic fibroblast growth factor, glial cell linederived neurotrophic factor, brain-derived neurotrophic factor, and ciliary neurotrophic factor are intimately involved in the maturation, maintenance and reinnervation of the MEPs and the recovery of motor function after denervation. [66][67][68][69][70][71][72] Therefore, local administration of these neurotrophic factors to the MEP zone in the target muscle may serve as a therapeutic option for preserving the denervated MEPs in the chronically denervated muscle. Preservation of MEPs for a longer period of time could enlarge the therapeutic time-window for NMEG-NMZ and promote functional recovery of the muscles with delayed reinnervation.…”

Heparin-based coacervate of bFGF facilitates peripheral nerve regeneration by inhibiting endoplasmic reticulum stress following sciatic nerve injury

“…In contrast to other NTFs that diffuse over relatively long distances [ 32 ], bFGF exhibits a variety of biological properties including neuroprotection, neurogenesis and angiogenesis in both the central nervous system (CNS) and peripheral nervous system (PNS). Previous research has demonstrated that endogenous bFGF increased the branching of transected axonsand promoted motor functionafter facial nerve cut [ 33 , 34 ]. However, in this study, we focus on the effect of exogenous bFGF, and intrathecal administration of bFGF could markedly alleviate functional recovery after acute spinal cord injury (SCI) [ 35 ].…”

FGF binding proteins (FGFBPs): Modulators of FGF signaling in the developing, adult, and stressed nervous system

“…Recombinant FGF2 increases the clustering of synaptic vesicles, an early cellular change at developing NMJs, when added to cultured motor neurons [49]. Additionally, FGF2 is important for the timely elimination of supernumerary axons innervating a single muscle fiber, a term often referred to as “synaptic elimination” [50–52]. In mice and rats, synaptic elimination ends around nine postnatal days (P9), but injection of FGF2 into rat gastrocnemius muscles at P2 slows the rate of synaptic elimination, and muscle fibers remain innervated by multiple motor axons until P14 [51].…”

“…It is therefore plausible that the levels of FGF2 at specific stages of development and secreted from unique cell types have different effects on the formation of the NMJ. In this regard, FGF2 levels have been found to correlate with different cellular changes associated with synaptic elimination [52], such as the arrival of the growing motor axon, the differentiation of the motor axon growth cone into a presynaptic site, and the reduction of nerve sprouts that migrate beyond the post-synaptic site. In addition to affecting the presynaptic region of the NMJ, FGF2 also affects the development of the postsynaptic region.…”