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首页> 外文期刊>Progress in brain research >Cell death in models of spinal cord injury.
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Cell death in models of spinal cord injury.

机译：脊髓损伤模型中的细胞死亡。

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摘要

Current treatments for acute spinal cord injury are based on animal models of human spinal cord injury (SCI). These models have shown that the initial traumatic injury to cord tissue is followed by a long period of secondary injury that includes a number of cellular and biochemical cascades. These secondary injury processes are potential targets for therapies. Continued refinement of rat and mouse models of SCI, along with more detailed analyses of the biology of the lesion in these models, points to both necrotic and apoptotic mechanisms of cell death after SCI. In this chapter, we review recent evidence for long-term apoptotic death of oligodendrocytes in long tracts undergoing Wallerian degeneration following SCI. This process appears to be related closely to activation of microglial cells. It is has been thought that microglial cells might be the source of cytotoxic cytokines, such as tumor necrosis factor-alpha (TNF-alpha), that kill oligodendrocytes. However, more recent evidence in vivo suggeststhat TNF-alpha by itself may not induce necrosis or apoptosis in oligodendrocytes. We review data that suggests other possible pathways for apoptosis, such as the neurotrophin receptor p75 which is expressed in both neurons and oligodendrocytes after SCI in rats and mice. In addition, it appears that microglial activation and TNF-alpha may be important in acute SCI. Ninety minutes after a moderate contusion lesion, microglia are activated and surround dying neurons. In an 'atraumatic' model of SCI, we have now shown that TNF-alpha appears to greatly potentiate cell death mediated by glutamate receptors. These studies emphasize that multiple mechanisms and interactions contribute to secondary injury after SCI. Continued study of both contusion models and other new approaches to studying these mechanisms will be needed to maximize strategies for acute and chronic therapies, and for neural repair.
机译：急性脊髓损伤的当前治疗是基于人脊髓损伤（SCI）的动物模型。这些模型表明，最初对脐带组织的创伤性损伤之后是长期的继发性损伤，包括许多细胞和生化级联反应。这些继发性损伤过程是治疗的潜在目标。对SCI大鼠和小鼠模型的不断完善，以及对这些模型中病变生物学的更详细分析，都指出了SCI后细胞死亡的坏死和凋亡机制。在本章中，我们回顾了SCI后经历Wallerian变性的长道中少突胶质细胞长期凋亡死亡的证据。这个过程似乎与小胶质细胞的激活密切相关。据认为，小胶质细胞可能是杀伤少突胶质细胞的细胞毒性细胞因子的来源，例如肿瘤坏死因子-α（TNF-α）。但是，体内的最新证据表明，TNF-α本身可能不会诱导少突胶质细胞坏死或凋亡。我们审查的数据表明凋亡的其他可能途径，如神经营养蛋白受体p75在大鼠和小鼠SCI后在神经元和少突胶质细胞中表达。此外，似乎小胶质细胞激活和TNF-α在急性SCI中可能很重要。中度挫伤性病变后90分钟，小胶质细胞被激活并围绕垂死的神经元。在SCI的“无创伤”模型中，我们现在显示TNF-α似乎大大增强了由谷氨酸受体介导的细胞死亡。这些研究强调SCI后继发性损伤的多种机制和相互作用。为了使急，慢性疗法和神经修复的策略最大化，需要继续研究挫伤模型和其他研究这些机制的新方法。

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