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

The EMBO Journal
Anne JacobiFlorence M Bareyre

Abstract

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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Citations

Dec 23, 2015·Neural Regeneration Research·Anne Jacobi, Florence M Bareyre
Nov 17, 2017·Neurodegenerative Disease Management·Martin Kerschensteiner
Jul 4, 2019·Journal of Molecular Neuroscience : MN·Jeremy McCallum-LoudeacMegan J Wilson
Aug 9, 2019·The Journal of Experimental Medicine·Peter M BradleyFlorence M Bareyre
Jun 28, 2019·Frontiers in Cellular Neuroscience·Hiroyuki KatohMichael G Fehlings
Mar 9, 2017·Frontiers in Cellular Neuroscience·Alexandra ChovsepianFlorence M Bareyre
Nov 1, 2020·Cellular and Molecular Life Sciences : CMLS·Kristina LoyFlorence M Bareyre
Aug 24, 2019·Neuroscience and Biobehavioral Reviews·Monokesh K SenPeter J Shortland
Apr 17, 2021·Molecular Neurobiology·Lars Klimaschewski, Peter Claus
May 4, 2021·Frontiers in Endocrinology·Giovanni VitaleAnnamaria Colao
Aug 15, 2021·Experimental Neurology·Valérie Van Steenbergen, Florence M Bareyre

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