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Publication : FGF22 signaling regulates synapse formation during post-injury remodeling of the spinal cord.

First Author  Jacobi A Year  2015
Journal  EMBO J Volume  34
Issue  9 Pages  1231-43
PubMed ID  25766255 Mgi Jnum  J:221040
Mgi Id  MGI:5637855 Doi  10.15252/embj.201490578
Citation  Jacobi A, et al. (2015) FGF22 signaling regulates synapse formation during post-injury remodeling of the spinal cord. EMBO J 34(9):1231-43
abstractText  The remodeling of axonal circuits after injury requires the formation of new synaptic contacts to enable functional recovery. Which molecular signals initiate such axonal and synaptic reorganisation in the adult central nervous system is currently unknown. Here, we identify FGF22 as a key regulator of circuit remodeling in the injured spinal cord. We show that FGF22 is produced by spinal relay neurons, while its main receptors FGFR1 and FGFR2 are expressed by cortical projection neurons. FGF22 deficiency or the targeted deletion of FGFR1 and FGFR2 in the hindlimb motor cortex limits the formation of new synapses between corticospinal collaterals and relay neurons, delays their molecular maturation, and impedes functional recovery in a mouse model of spinal cord injury. These results establish FGF22 as a synaptogenic mediator in the adult nervous system and a crucial regulator of synapse formation and maturation during post-injury remodeling in the spinal cord.
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