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轴突切断术会导致细胞内游离钙浓度短暂且局部地升高至毫摩尔范围。

Axotomy induces a transient and localized elevation of the free intracellular calcium concentration to the millimolar range.

作者信息

Ziv N E, Spira M E

机构信息

Department of Neurobiology, Hebrew University of Jerusalem, Israel.

出版信息

J Neurophysiol. 1995 Dec;74(6):2625-37. doi: 10.1152/jn.1995.74.6.2625.

Abstract
  1. Axonal transection triggers a cascade of pathological processes that frequently lead to the degeneration of the injured neuron. It is generally believed that the degenerative process is triggered by an overwhelming influx of calcium through the cut end of the axon. 2. Theoretical considerations and indirect observations suggest that axotomy is followed by an increase in the free intracellular calcium concentration ([Ca2+]i) to the millimolar level. In contrast, only relatively modest and transient elevation in [Ca2+]i to the micromolar level was revealed by recent fura-2 studies. 3. In the current study we used the low-affinity Ca2+ indicator mag-fura-2 to reexamine the spatiotemporal distribution pattern of Ca2+ after axotomy and to map the free intracellular Mg2+ concentration gradients. 4. We report that axotomy elevates [Ca2+]i well beyond the "physiological" range of calcium concentrations, to levels > 1 mM near the tip of the cut axon and to hundreds of micromolars along the axon further away from the cut end. Nevertheless, [Ca2+]i recovers to the control levels within 2-3 min after the resealing of the cut end. 5. A comparison of the behavior of fura-2 and mag-fura-2 in the cytosol of the axotomized neurons reveals that the determination of [Ca2+]i by fura-2 largely underestimates the actual intracellular Ca2+ concentrations. 6. Experiments in which one branch of a bifurcated axon was transected revealed that the elevation in [Ca2+]i is confined to the transected axonal branch and does not spread beyond the bifurcation point. 7. After axotomy, the intracellular Mg2+ concentration equilibrates rapidly with the external concentration and then recovers at a rate somewhat slower than that of [Ca2+]i. 8. To the best of our knowledge, this study is the first direct demonstration that axotomy elevates [Ca2+]i to the millimolar range and that neurons are able to recover from these extreme calcium concentrations.
摘要
  1. 轴突横断引发一系列病理过程,这些过程常常导致受损神经元变性。一般认为,变性过程是由钙通过轴突断端大量内流所触发的。2. 理论思考和间接观察表明,轴突切断后细胞内游离钙浓度([Ca2+]i)会升高至毫摩尔水平。相比之下,近期使用fura-2的研究仅揭示了[Ca2+]i相对适度且短暂地升高至微摩尔水平。3. 在本研究中,我们使用低亲和力钙指示剂mag-fura-2重新检查轴突切断后钙的时空分布模式,并绘制细胞内游离镁离子浓度梯度图。4. 我们报告称,轴突切断使[Ca2+]i升高至远超钙浓度的“生理”范围,在切断轴突尖端附近达到>1 mM的水平,在远离断端的轴突上达到数百微摩尔。然而,在断端重新封闭后2 - 3分钟内,[Ca2+]i恢复到对照水平。5. 对轴突切断神经元胞质中fura-2和mag-fura-2行为的比较表明,fura-2对[Ca2+]i的测定在很大程度上低估了实际细胞内钙浓度。6. 对分叉轴突的一个分支进行横断的实验表明,[Ca2+]i的升高局限于横断的轴突分支,不会扩散到分叉点之外。7. 轴突切断后,细胞内镁离子浓度迅速与外部浓度平衡,然后以略慢于[Ca2+]i恢复的速率恢复。8. 据我们所知,本研究首次直接证明轴突切断使[Ca2+]i升高至毫摩尔范围,并且神经元能够从这些极端钙浓度中恢复。

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