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Journal of NeuroscienceVolume 34, Issue 17, 2014, Pages 5965-5970

CNS axons globally increase axonal transport after peripheral conditioning(Article)(Open Access)

  • Mar, F.M.,
  • Simões, A.R.,
  • Leite, S.,
  • Morgado, M.M.,
  • Santos, T.E.,
  • Rodrigo, I.S.,
  • Teixeira, C.A.,
  • Misgeld, T.,
  • Sousa, M.M.
  • View Correspondence (jump link)
  • aNerve Regeneration Group, Instituto de Biologia Molecular e Celular (IBMC), University of Porto, 4150-180 Porto, Portugal
  • bInstituto de Ciências Biomédicas Abel Salazar (ICBAS), 4050-313 Porto, Portugal
  • cInstitute of Neuronal Cell Biology, Munich Cluster for Systems Neurology and German Center for Neurodegenerative Diseases, Technische Universität München, 80802 München, Germany

Abstract

Despite the inability of CNS axons to regenerate, an increased regenerative capacity can be elicited following conditioning lesion to the peripheral branch of dorsal root ganglia neurons (DRGs). By in vivo radiolabeling of rat DRGs, coupled to mass spectrometry and kinesin immunoprecipitation of spinal cord extracts, we determined that the anterograde transport of cytoskeleton components, metabolic enzymes and axonal regeneration enhancers, was increased in the central branch of DRGs following a peripheral conditioning lesion. Axonal transport of mitochondria was also increased in the central branch of Thy1-MitoCFP mice following a peripheral injury. This effect was generalized and included augmented transport of lysosomes and synaptophysin- and APP-carrying vesicles. Changes in axonal transport were only elicited by a peripheral lesion and not by spinal cord injury. In mice, elevated levels of motors and of polyglutamylated and tyrosinated tubulin were present following a peripheral lesion and can explain the increase in axonal transport induced by conditioning. In summary, our work shows that a peripheral injury induces a global increase in axonal transport that is not restricted to the peripheral branch, and that, by extending to the central branch, allows a rapid and sustained support of regenerating central axons. © 2014 the authors.

Author keywords

Axon regenerationAxonal transportConditioning lesion

Indexed keywords

EMTREE drug terms:actinAnxa5 proteinCRMP 5 proteindynein 1 proteinkinesinpeptides and proteinsPGP9.5 proteinRho guanine nucleotide dissociation inhibitorsynaptophysintubulinunclassified drug
EMTREE medical terms:animal experimentanimal modelarticlecentral nervous systemcontrolled studygene expressionimmunoprecipitationlysosomemass spectrometrymitochondrionnerve cell lesionnerve fibernerve fiber growthnerve fiber transportnonhumanperipheral nervepriority journalprotein expressionprotein phosphorylationratreal time polymerase chain reactionsciatic nerve injuryspinal cord injuryspinal ganglionWestern blotting
Medline keywords:axon regenerationaxonal transportconditioning lesion
MeSH:AnimalsAxonal TransportAxonsCyclic AMPGanglia, SpinalLysosomesMiceMice, TransgenicMitochondriaNerve RegenerationNeuronsRatsRats, WistarSynaptophysin
  • ISSN: 02706474
  • CODEN: JNRSD
  • Source Type: Journal
  • Original language: English
  • DOI: 10.1523/JNEUROSCI.4680-13.2014
  • PubMed ID: 24760855
  • Document Type: Article
  • Publisher: Society for Neuroscience

  Sousa, M. M.; Nerve Regeneration Group, IBMC, Rua do Campo Alegre 823, Portugal;
© Copyright 2014 Elsevier B.V., All rights reserved.

Cited by 38 documents

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An In Vitro Model for Conditioning Lesion Effect
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Walker, C.L. , Uchida, A. , Li, Y.
Local acceleration of neurofilament transport at nodes of ranvier
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View details of all 38 citations
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