Evidence map›Paper›PMID 26586827›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1-/- Mice.

Kathren L Fink, Stephen M Strittmatter, William B J Cafferty

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. Single-Nuclei Sequencing Reveals a Robust Corticospinal Response to Nearby Axotomy But Overall Insensitivity to Spinal Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  4. Article
  5. Injury distance limits the transcriptional response to spinal injury.bioRxiv : the preprint server for biology · 2024
    Article
  6. Article
  7. Article
  8. Anatomical Diversity of the Adult Corticospinal Tract Revealed by Single-Cell Transcriptional Profiling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Single Nuclei Analyses Reveal Transcriptional Profiles and Marker Genes for Diverse Supraspinal Populations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  10. Article
  11. Inositol Polyphosphate-5-Phosphatase K (The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Modulation of Both Intrinsic and Extrinsic Factors Additively Promotes Rewiring of Corticospinal Circuits after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. iScience · 2021
    Article
  17. Article
  18. Review
  19. Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Kathren L FinkDepartment of Neurology and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, Connecticut 06520.ORCID http://orcid.org/0000-0002-2956-4454
Stephen M StrittmatterDepartment of Neurology and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, Connecticut 06520 william.cafferty@yale.edu stephen.strittmatter@yale.edu.ORCID http://orcid.org/0000-0001-8188-3092
William B J CaffertyDepartment of Neurology and william.cafferty@yale.edu stephen.strittmatter@yale.edu.ORCID http://orcid.org/0000-0001-6263-2167
Yale University · US

Funding

PRG3 drives functional plasticity in intact circuits after spinal cord injuryR01NS095930 · NINDS · YALE UNIVERSITY · PI CAFFERTY, WILLIAM B. · 2016 to 2020
$1.8M
Cortical Plasticity during Recovery from Spinal Cord InjuryR01NS080388 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2012 to 2016
$1.8M
Functional Genomics of Axonal and Synapse RegenerationR33NS079306 · NINDS · YALE UNIVERSITY · PI STRITTMATTER, STEPHEN M · 2013 to 2014
$1.4M
NINDS NIH HHS R01 NS080388NINDS NIH HHS R01NS080388NINDS NIH HHS R01 NS095930NINDS NIH HHS R33 NS079306
6 · The paper itself

Abstract

Spinal cord injury interrupts descending motor tracts and creates persistent functional deficits due to the absence of spontaneous axon regeneration. Of descending pathways, the corticospinal tract (CST) is thought to be the most critical for voluntary function in primates. Even with multiple tracer injections and genetic tools, the CST is visualized to only a minor degree in experimental studies. Here, we identify and validate the mu-crystallin (crym) gene as a high-fidelity marker of the CST. In transgenic mice expressing green fluorescent protein (GFP) under crym regulatory elements (crym-GFP), comprehensive and near complete CST labeling is achieved throughout the spinal cord. Bilateral pyramidotomy eliminated the 17,000 GFP-positive CST axons that were reproducibly labeled in brainstem from the spinal cord. We show that CST tracing with crym-GFP is 10-fold more efficient than tracing with biotinylated dextran amine (BDA). Using crym-GFP, we reevaluated the CST in mice lacking nogo receptor 1 (NgR1), a protein implicated in limiting neural repair. The number and trajectory of CST axons in ngr1(-/-) mice without injury was indistinguishable from ngr1(+/+) mice. After dorsal hemisection in the midthoracic cord, CST axons did not significantly regenerate in ngr1(+/+) mice, but an average of 162 of the 6000 labeled thoracic CST axons (2.68%) regenerated >100 μm past the lesion site in crym-GFP ngr1(-/-) mice. Although traditional BDA tracing cannot reliably visualize regenerating ngr1(-/-) CST axons, their regenerative course is clear with crym-GFP. Therefore the crym-GFP transgenic mouse is a useful tool for studies of CST anatomy in experimental studies of motor pathways. SIGNIFICANCE STATEMENT: Axon regeneration fails in the adult CNS, resulting in permanent functional deficits. Traditionally, inefficient extrinsic tracers such a biotinylated dextran amine (BDA) are used to label regenerating fibers after therapeutic intervention. We introduce crym-green fluorescent protein (GFP) transgenic mice as a comprehensive and specific tool with which to study the primary descending motor tract, the corticospinal tract (CST). CST labeling with crym-GFP is 10 times more efficient compared with BDA. The enhanced sensitivity afforded by crym-GFP revealed significant CST regeneration in NgR1 knock-out mice. Therefore, crym-GFP can be used as a standardized tool for future CST spinal cord injury studies.

Indexed as

AmidinesAnalysis of VarianceAnimalsAxonsBiotinCrystallinsDextransDisease Models, AnimalFunctional LateralityGene Expression RegulationGlial Fibrillary Acidic ProteinGPI-Linked ProteinsLuminescent ProteinsMiceMice, Inbred C57BLMice, TransgenicAmidinesBiotinbiotinylated dextran amineCrym protein, mouseCrystallinsDextransdiamidino compound 253-50Glial Fibrillary Acidic ProteinGPI-Linked ProteinsLuminescent Proteinsmu-CrystallinsMyelin ProteinsNogo Receptor 1Receptors, Cell SurfaceRtn4r protein, mousecorticospinal tractnogo receptorregenerationspinal cord injurytransgene

Identifiers

PMID26586827
PMCPMC4649010
OpenAlexW2344551930

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.