RESPONSES OF THE NERVE CELL BODY TO AXOTOMY
RESPONSES OF THE NERVE CELL BODY TO AXOTOMY
复制标题
神经细胞体对轴切术的反应
DOI:
10.1227/01.neu.0000352378.26755.c3
复制
发表时间:
2009
期刊:
影响因子:
4.8
通讯作者:
X. Bo
中科院分区:
文献类型:
--
作者:
P. Richardson;Tizong Miao;Dongsheng Wu;Yi Zhang;J. Yeh;X. Bo
OBJECTIVEPeripheral nerve injury causes retrograde changes in the damaged neurons, which are beneficial to axonal regeneration. Better understanding of the mechanisms of induction and mediation of these conditioning responses would help to design strategies to invoke stronger regenerative responses in neurons in situations when these responses are inadequate. METHODSRelevant literature is reviewed. RESULTSExperimental preparations that measure the influence of peripheral axotomy on regeneration in the central axons of primary sensory neurons are useful to examine mechanisms of conditioning neurons. Despite 4 decades of speculation, the nature of the damage signals from injured nerves that initiate axonal signals to the nerve cell body remains elusive. Members of the family of neuropoietic cytokines are clearly implicated, but what induces them is unknown. Multiple changes in gene regulation in axotomized neurons have been described, and dozens of growth-associated genes have been identified: neurotrophic factors, transcription factors, molecules participating in axonal transport, and molecules active in the growth cone. The mechanisms of interaction of a few regeneration-associated molecules with the signaling cascades that lead to actin and tubulin remodeling at the growth cone are understood in some detail. In animals, viral gene therapy to deliver regeneration-associated genes to neurons or other local measures to induce these genes can improve regeneration. A few pharmacological agents, administered systemically, have small beneficial effects on axonal regeneration. CONCLUSIONAdvances in laboratory research have provided knowledge of cell body responses to axotomy with clinical relevance.
影响因子:
2.4
作者:
Costigan M;Befort K;Karchewski L;Griffin RS;D'Urso D;Allchorne A;Sitarski J;Mannion JW;Pratt RE;Woolf CJ
通讯作者:
Woolf CJ