Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, Jiangsu, China.
Department of Pathology, Nantong University Affiliated Hospital, Nantong, Jiangsu, China.
Mol Neurobiol. 2024 Jan;61(1):423-433. doi: 10.1007/s12035-023-03590-7. Epub 2023 Aug 24.
Peripheral nerves obtain remarkable regenerative capacity while central nerves can hardly regenerate following nerve injury. Sensory neurons in the dorsal root ganglion (DRG) are widely used to decipher the dissimilarity between central and peripheral axonal regeneration as axons of DRG neurons bifurcate into the regeneration-incompetent central projections and the regeneration-competent peripheral projections. A conditioning peripheral branch injury facilitates central axonal regeneration and enables the growth and elongation of central axons. Peripheral axonal injury stimulates neuronal calcium influx, alters the start-point chromatin states, increases chromatin accessibility, upregulates the expressions of regeneration-promoting genes and the synthesis of proteins, and supports axonal regeneration. Following central axonal injury, the responses of DRG neurons are modest, resulting in poor intrinsic growth ability. Some non-neuronal cells in DRGs, for instance satellite glial cells, also exhibit diminished injury responses to central axon injury as compared with peripheral axon injury. Moreover, DRG central and peripheral axonal branches are respectively surrounded by inhibitory glial scars generated by central glial cells and a permissive microenvironment generated by Schwann cells and macrophages. The aim of this review is to look at changes of DRG neurons and non-neuronal cells after peripheral and central axon injuries and summarize the contributing roles of both neuronal intrinsic regenerative capacities and surrounding microenvironments in axonal regeneration.
周围神经具有显著的再生能力,而中枢神经在神经损伤后几乎无法再生。背根神经节 (DRG) 中的感觉神经元被广泛用于破译中枢和周围轴突再生之间的差异,因为 DRG 神经元的轴突分叉为再生能力差的中枢投射和再生能力强的周围投射。周围分支损伤可以促进中枢轴突再生,并使中枢轴突生长和伸长。周围轴突损伤刺激神经元钙内流,改变起始点染色质状态,增加染色质可及性,上调促进再生的基因表达和蛋白质合成,支持轴突再生。中枢轴突损伤后,DRG 神经元的反应较小,导致内在生长能力较差。DRG 中的一些非神经元细胞,如卫星胶质细胞,对中枢轴突损伤的反应也比周围轴突损伤小。此外,DRG 的中枢和周围轴突分支分别被中枢胶质细胞产生的抑制性胶质瘢痕和 Schwann 细胞和巨噬细胞产生的允许性微环境所包围。本综述的目的是观察周围和中枢轴突损伤后 DRG 神经元和非神经元细胞的变化,并总结神经元内在再生能力和周围微环境在轴突再生中的作用。