作者: Nicholas J. Batty , Keith K. Fenrich , Karim Fouad
DOI: 10.1016/J.NEULET.2016.12.033
关键词: Nervous system 、 Neuron 、 Central nervous system 、 Effector 、 Kinase 、 Biology 、 Neurite 、 Growth cone 、 Downregulation and upregulation 、 Neuroscience
摘要: Abstract Injured neurons in the adult mammalian central nervous system (CNS) have a very limited capacity for axonal regeneration and neurite outgrowth. This inability to grow new axons or regrow injured is due presence of molecules that inhibit growth, age related changes neuron’s innate growth capabilities. Available levels cAMP are thought an important role linking both these factors. Elevated developing guidance stability cones. As matures, decline promoting effects diminish. It has frequently been demonstrated increasing neuronal can enhance regeneration. Some methods used increase include administration agonists, conditioning lesions, electrical stimulation. Furthermore, it proposed multiple stages induced exist, one directly caused by its downstream effector Protein Kinase A (PKA) eventual upregulation gene transcription. Although axon well accepted, pathways mediate cAMP-mediated less clear. partly because various key studies explored link between PKA outgrowth relied on inhibitors KT5720 H89. More recent shown drugs specific than initially number other signalling including Exchange Activated (EPAC). Consequently, recently intracellular previously attributed now be solely activation EPAC pathways, simultaneous co-activation pathways. These open door potential treatments repairing spinal cord.