PUBLICATION

Developmentally Regulated Impediments to Skin Reinnervation by Injured Peripheral Sensory Axon Terminals

Authors
O'Brien, G.S., Martin, S.M., Söllner, C., Wright, G.J., Becker, C.G., Portera-Cailliau, C., and Sagasti, A.
ID
ZDB-PUB-091215-44
Date
2009
Source
Current biology : CB   19(24): 2086-2090 (Journal)
Registered Authors
Becker, Catherina G., O'Brien, Georgeann, Sagasti, Alvaro, Söllner, Christian, Wright, Gavin J.
Keywords
MOLNEURO
MeSH Terms
  • Animals
  • Axotomy
  • DNA Primers/genetics
  • DNA, Complementary/genetics
  • Microscopy, Confocal
  • Mutagenesis, Site-Directed
  • Nerve Regeneration/physiology*
  • Neuronal Plasticity/physiology*
  • Presynaptic Terminals/physiology*
  • Receptors, Cell Surface/genetics
  • Receptors, Cell Surface/metabolism
  • Sensory Receptor Cells/physiology*
  • Skin/innervation*
  • Trigeminal Nerve/cytology*
  • Trigeminal Nerve Injuries
  • Zebrafish
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • rhoA GTP-Binding Protein/metabolism
(all 19)
PubMed
19962310 Full text @ Curr. Biol.
Abstract
The structural plasticity of neurites in the central nervous system (CNS) diminishes dramatically after initial development, but the peripheral nervous system (PNS) retains substantial plasticity into adulthood. Nevertheless, functional reinnervation by injured peripheral sensory neurons is often incomplete [1-6]. To investigate the developmental control of skin reinnervation, we imaged the regeneration of trigeminal sensory axon terminals in live zebrafish larvae following laser axotomy. When axons were injured during early stages of outgrowth, regenerating and uninjured axons grew into denervated skin and competed with one another for territory. At later stages, after the establishment of peripheral arbor territories, the ability of uninjured neighbors to sprout diminished severely, and although injured axons reinitiated growth, they were repelled by denervated skin. Regenerating axons were repelled specifically by their former territories, suggesting that local inhibitory factors persist in these regions. Antagonizing the function of several members of the Nogo receptor (NgR)/RhoA pathway improved the capacity of injured axons to grow into denervated skin. Thus, as in the CNS, impediments to reinnervation in the PNS arise after initial establishment of axon arbor structure.
Genes / Markers
Marker Marker Type Name
dpysl2bGENEdihydropyrimidinase like 2b
dpysl3GENEdihydropyrimidinase like 3
lingo1aGENEleucine rich repeat and Ig domain containing 1a
neurog1GENEneurogenin 1
rhoabGENEras homolog gene family, member Ab
rtn4rGENEreticulon 4 receptor
1 - 6 of 6
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Figures
Figure Gallery (7 images)
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Expression
Phenotype
Fish Conditions Stage Phenotype Figure
WT + MO1-dpysl2bablation: axon: trigeminal ganglionProtruding-mouth
WT + MO1-lingo1aablation: axon: trigeminal ganglionProtruding-mouth
WT + MO6-neurog1ablation: axon: trigeminal ganglionProtruding-mouth
1 - 3 of 3
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Mutations / Transgenics
Allele Construct Type Affected Genomic Region
zc7TgTransgenic Insertion
    zf154TgTransgenic Insertion
      zf234TgTransgenic Insertion
        1 - 3 of 3
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        Human Disease / Model
        No data available
        Sequence Targeting Reagents
        Target Reagent Reagent Type
        dpysl2bMO1-dpysl2bMRPHLNO
        lingo1aMO1-lingo1aMRPHLNO
        neurog1MO6-neurog1MRPHLNO
        rtn4rMO1-rtn4rMRPHLNO
        1 - 4 of 4
        Show
        Fish
        Fish
        WT + MO1-dpysl2b
        WT + MO1-lingo1a
        WT + MO6-neurog1
        zc7Tg
        zf154Tg
        zf234Tg
        1 - 6 of 6
        Show
        Antibodies
        Orthology
        Engineered Foreign Genes
        Marker Marker Type Name
        EGFPEFGEGFP
        GAL4EFGGAL4
        GFPEFGGFP
        RFPEFGRFP
        1 - 4 of 4
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        Mapping
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        Citation
        O'Brien, G.S., Martin, S.M., Söllner, C., Wright, G.J., Becker, C.G., Portera-Cailliau, C., and Sagasti, A. (2009) Developmentally Regulated Impediments to Skin Reinnervation by Injured Peripheral Sensory Axon Terminals. Current biology : CB. 19(24):2086-2090.