Comparison of regenerative neurogenesis in response to CNS injury between adult zebrafish and mice

Kuan Chung
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引用次数: 1

Abstract

The difference between adult zebrafish and mice in their regenerative capacity following central nervous system (CNS) injury is influenced by the permissiveness of the brain microenvironment aside from the intrinsic neurogenic potential of the cell population. In adult zebrafish, glia cells largely retain their radial characteristics and neurogenic capacity, and the zebrafish brain shows full recovery after traumatic brain injury (TBI) as well as spinal cord injury (SCI). Conversely, in mice, radial glia (RG) have largely differentiated into astrocytes. Excluding certain brain regions, following TBI, reactive astrocytes that show the potential to become neural stem cells (NSCs) in vitro remain strictly non-neurogenic in vivo due to the presence of inhibitory factors in the microenvironment. Combined with prolonged inflammation and gliosis, injury to the CNS eventually results in formation of a glial scar further impeding regeneration. However in rodents, suppression of neurogenesis may be a protection mechanism against possible detrimental side-effects of neurogenesis in the long term.
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成年斑马鱼与小鼠中枢神经系统损伤后再生神经发生的比较
成年斑马鱼和小鼠在中枢神经系统(CNS)损伤后再生能力的差异除了受细胞群固有神经源性的影响外,还受脑微环境的容纳性的影响。在成年斑马鱼中,神经胶质细胞在很大程度上保留了其径向特征和神经发生能力,斑马鱼的大脑在创伤性脑损伤(TBI)和脊髓损伤(SCI)后表现出完全的恢复。相反,在小鼠中,径向胶质细胞(RG)大部分分化为星形胶质细胞。排除脑外伤后的某些脑区,由于微环境中存在抑制因子,在体外表现出成为神经干细胞(NSCs)潜力的反应性星形胶质细胞在体内严格保持非神经源性。再加上长期的炎症和神经胶质瘤,中枢神经系统的损伤最终导致神经胶质瘤疤痕的形成,进一步阻碍再生。然而,在啮齿类动物中,抑制神经发生可能是一种长期的保护机制,可以防止神经发生可能产生的有害副作用。
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