Literature DB >> 8747220

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

N E Ziv1, M E Spira.   

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.

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Year:  1995        PMID: 8747220     DOI: 10.1152/jn.1995.74.6.2625

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


  44 in total

1.  Barrier permeability at cut axonal ends progressively decreases until an ionic seal is formed.

Authors:  C S Eddleman; G D Bittner; H M Fishman
Journal:  Biophys J       Date:  2000-10       Impact factor: 4.033

Review 2.  Assembly of a new growth cone after axotomy: the precursor to axon regeneration.

Authors:  Frank Bradke; James W Fawcett; Micha E Spira
Journal:  Nat Rev Neurosci       Date:  2012-02-15       Impact factor: 34.870

3.  Roles of membrane trafficking in nerve repair and regeneration.

Authors:  Elizabeth Tuck; Valeria Cavalli
Journal:  Commun Integr Biol       Date:  2010-05

4.  Retrograde and Wallerian axonal degeneration occur synchronously after retinal ganglion cell axotomy.

Authors:  Akiyasu Kanamori; Maria-Magdalena Catrinescu; Jonathan M Belisle; Santiago Costantino; Leonard A Levin
Journal:  Am J Pathol       Date:  2012-05-26       Impact factor: 4.307

Review 5.  Molecular and Cellular Mechanisms of Axonal Regeneration After Spinal Cord Injury.

Authors:  Erna A van Niekerk; Mark H Tuszynski; Paul Lu; Jennifer N Dulin
Journal:  Mol Cell Proteomics       Date:  2015-12-22       Impact factor: 5.911

6.  WldS and PGC-1α regulate mitochondrial transport and oxidation state after axonal injury.

Authors:  Kelley C O'Donnell; Mauricio E Vargas; Alvaro Sagasti
Journal:  J Neurosci       Date:  2013-09-11       Impact factor: 6.167

7.  Sodium and potassium currents influence Wallerian degeneration of injured Drosophila axons.

Authors:  Bibhudatta Mishra; Ross Carson; Richard I Hume; Catherine A Collins
Journal:  J Neurosci       Date:  2013-11-27       Impact factor: 6.167

8.  Axon regeneration genes identified by RNAi screening in C. elegans.

Authors:  Paola Nix; Marc Hammarlund; Linda Hauth; Martina Lachnit; Erik M Jorgensen; Michael Bastiani
Journal:  J Neurosci       Date:  2014-01-08       Impact factor: 6.167

Review 9.  Axon-soma communication in neuronal injury.

Authors:  Ida Rishal; Mike Fainzilber
Journal:  Nat Rev Neurosci       Date:  2013-12-11       Impact factor: 34.870

10.  Calcium-activated proteases are critical for refilling depleted vesicle stores in cultured sensory-motor synapses of Aplysia.

Authors:  Arkady Khoutorsky; Micha E Spira
Journal:  Learn Mem       Date:  2005 Jul-Aug       Impact factor: 2.460

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