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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Spatiotemporal distribution of spectrin breakdown products induced by anoxia in adult rat optic nerve in vitro.
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Spatiotemporal distribution of spectrin breakdown products induced by anoxia in adult rat optic nerve in vitro.

机译：缺氧在成年大鼠视神经中诱发的血影蛋白分解产物的时空分布。

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Hypoxic/ischemic and traumatic injury to central nervous system myelinated axons is heavily dependent on accumulation of Ca ions in the axoplasm, itself promoted by Na influx from the extracellular space. Given the high density of nodal Na channels, we hypothesized that nodes of Ranvier might be particularly vulnerable to Ca overload and subsequent damage, as this is the expected locus of maximal Na influx. Adult rat optic nerves were exposed to in vitro anoxia and analyzed immunohistochemically for the presence of spectrin breakdown. Cleavage of spectrin became detectable between 15 and 30 mins of anoxia, and increased homogeneously along the lengths of fibers; localized breakdown was not observed at nodes of Ranvier at any time point analyzed. Spectrin breakdown was also found in glial processes surrounding axons. Confocal imaging of axoplasmic Ca also revealed a gradual and nonlocalized increase as anoxia progressed, without evidence of Ca 'hot-spots' anywhere along the axons at any time between 0 and 30 mins of anoxic exposure in vitro. Calculations of Ca diffusion rates indicated that even if Ca entered or was released focally in axons, this ion would diffuse rapidly into the internodes and likely produce diffuse injury by activating Ca-dependent proteases. Western blot analysis for voltage-gated Na channel protein revealed that key functional proteins such as these are also degraded by anoxia/ischemia. Thus, proteolysis of structural and functional proteins will conspire to irreversibly injure central axons and render them nonfunctional, eventually leading to transection, degradation, and Wallerian degeneration.
机译：中枢神经系统髓鞘轴突的缺氧/缺血性和创伤性损伤严重依赖于钙离子在轴质中的积累，而钙离子本身是由来自细胞外空间的钠流入促进的。鉴于节点Na通道的密度很高，我们假设Ranvier的节点可能特别容易受到Ca超载和随后的破坏的影响，因为这是最大Na流入的预期场所。将成年大鼠的视神经暴露于体外缺氧，并通过免疫组织化学分析血影蛋白的存在。在缺氧的15分钟到30分钟之间可以检测到血影蛋白的裂解，并且沿纤维的长度均匀地增加。在任何时间点分析都未在Ranvier的节点上观察到局部故障。在轴突周围的神经胶质过程中也发现了血影蛋白的分解。共轴成像的轴质Ca也显示出随着缺氧的进行而逐渐的和非局部的增加，没有证据表明在体外缺氧暴露的0至30分钟之间的任何时间，沿轴突的任何地方都存在Ca“热点”。 Ca扩散速率的计算表明，即使Ca进入轴突或在轴突中被局部释放，该离子也将迅速扩散到节间，并可能通过激活Ca依赖性蛋白酶而产生弥散性损伤。电压门控Na通道蛋白的蛋白质印迹分析表明，缺氧/缺血也可降解诸如此类的关键功能蛋白。因此，结构蛋白和功能蛋白的蛋白水解作用将不可逆转地损害中央轴突并使它们失去功能，最终导致横切，降解和沃勒变性。

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