Inactivation of Glycogen Synthase Kinase 3 Promotes Axonal Growth and Recovery in the CNS

Axonal regeneration is minimal after CNS injuries in adult mammals and medical treatments to recover neurological deficits caused by axon disconnection are extremely limited. The failure of axonal elongation is principally attributed to the nonpermissive environment and reduced intrinsic growth capa...

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Veröffentlicht in:	The Journal of neuroscience 2008-09, Vol.28 (36), p.8914-8928
Hauptverfasser:	Dill, John, Wang, Hongyu, Zhou, Fengquan, Li, Shuxin
Format:	Artikel
Sprache:	eng
Schlagworte:	Aminophenols - pharmacology Animals Axons - drug effects Axons - physiology Behavior, Animal Cells, Cultured Central Nervous System - cytology Cerebellum - cytology Chondroitin Sulfate Proteoglycans - pharmacology Disease Models, Animal Enzyme Inhibitors - pharmacology Ganglia, Spinal - cytology Glycogen Synthase Kinase 3 - physiology Lithium - pharmacology Locomotion - drug effects Locomotion - physiology Maleimides - pharmacology Mice Mice, Inbred C57BL Nerve Tissue Proteins - metabolism Neurons - cytology Proto-Oncogene Proteins c-akt - metabolism Rats Recovery of Function - drug effects Recovery of Function - physiology Serotonin - metabolism Spinal Cord Injuries - drug therapy Spinal Cord Injuries - pathology Spinal Cord Injuries - physiopathology Time Factors
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