Neuritin: A therapeutic candidate for promoting axonal regeneration  

作　　者：Tadayuki Shimada Hiroko Sugiura Kanato Yamagata 

机构地区：[1]Neural Plasticity Project, Tokyo Metropolitan Institute of Medical Science

出　　处：《World Journal of Neurology》2013年第4期138-143,共6页世界神经病学杂志

基　　金：Supported by JSPS KAKENHI partly,No.24700349,No.24659093,No.25293239;MEXT KAKENHI,No.25110737

摘　　要：Following injury, the axons of the mammalian central nervous system do not regenerate. Many studies have aimed at understanding the mechanisms that prevent axonal regeneration and at designing ways to overcome the obstacles preventing axonal regrowth. These studies have identified numerous proteins as promoters of axonal regeneration. In this minireviews, we focus on neuritin as a therapeutic candidate for promoting axonal regeneration. Neuritin was first identified as a neuronal-activity-inducible gene product in the rat brain. The overexpression of neuritin in neurons or the application of neuritin to neurons induces neuritogenesis, neurite arborization, and axonal elongation both in vitro and in vivo. These morphological changes are often observed during the first step of axonal regeneration. Indeed, neuritin expression increases during axonal regeneration in the peripheral nervous system(PNS). Conversely, in a mouse model of diabetes mellitus, neuritin expression decreases in the PNS, and this reduced expression may result in deficient axonal regeneration. Neuritin is induced in the hippocampal dentate gyrus after temporal lobe epilepsy or brain ischemia; however, in these conditions, neuritin induc-tion may exacerbate brain dysfunction through mossy fiber sprouting. Together, these findings support the hypothesis that tightly controlled regulation of neuritin may be required for the treatment of each unique axonal pathology.Following injury, the axons of the mammalian central nervous system do not regenerate. Many studies have aimed at understanding the mechanisms that prevent axonal regeneration and at designing ways to overcome the obstacles preventing axonal regrowth. These studies have identified numerous proteins as promoters of axonal regeneration. In this minireviews, we focus on neuritin as a therapeutic candidate for promoting axonal regeneration. Neuritin was first identified as a neuronal-activity-inducible gene product in the rat brain. The overexpression of neuritin in neurons or the application of neuritin to neurons induces neuritogenesis, neurite arborization, and axonal elongation both in vitro and in vivo. These morphological changes are often observed during the first step of axonal regeneration. Indeed, neuritin expression increases during axonal regeneration in the peripheral nervous system(PNS). Conversely, in a mouse model of diabetes mellitus, neuritin expression decreases in the PNS, and this reduced expression may result in deficient axonal regeneration. Neuritin is induced in the hippocampal dentate gyrus after temporal lobe epilepsy or brain ischemia; however, in these conditions, neuritin induc-tion may exacerbate brain dysfunction through mossy fiber sprouting. Together, these findings support the hypothesis that tightly controlled regulation of neuritin may be required for the treatment of each unique axonal pathology.

关 键 词：AXONAL regeneration NEURONAL development AXONAL injury NEURITOGENESIS EPILEPSY 

分 类 号：R[医药卫生]