作者: Anne Jacobi , Kristina Loy , Anja M Schmalz , Mikael Hellsten , Hisashi Umemori
关键词:
摘要: The remodeling of axonal circuits after injury requires the formation new synaptic contacts to enable functional recovery. Which molecular signals initiate such and reorganisation in adult central nervous system is currently unknown. Here, we identify FGF22 as a key regulator circuit injured spinal cord. We show that produced by relay neurons, while its main receptors FGFR1 FGFR2 are expressed cortical projection neurons. deficiency or targeted deletion hindlimb motor cortex limits synapses between corticospinal collaterals delays their maturation, impedes recovery mouse model cord injury. These results establish synaptogenic mediator crucial synapse maturation during post-injury