Evidence map›Paper›PMID 21995852›Full record

ArticleThe European journal of neuroscience2011

Combined delivery of Nogo-A antibody, neurotrophin-3 and the NMDA-NR2d subunit establishes a functional 'detour' in the hemisected spinal cord.

Lisa Schnell, Arsen S Hunanyan, William J Bowers, Philip J Horner, Howard J Federoff, Miriam Gullo, Martin E Schwab, Lorne M Mendell, Victor L Arvanian

Open access · bronzeAbstract read
In one paragraph

Article in The European journal of neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Pericytes Act as Key Players in Spinal Cord Injury.The American journal of pathology · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Complement protein C1q modulates neurite outgrowth in vitro and spinal cord axon regeneration in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  13. Article
  14. Article
  15. Bridging the gap: a reticulo-propriospinal detour bypassing an incomplete spinal cord injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  16. Review
  17. Neurotrophins and spinal circuit function.Frontiers in neural circuits · 2014
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Lisa SchnellBrain Research Institute, University and ETH of Zurich, Zurich, Switzerland.
Arsen S Hunanyan
William J Bowers
Philip J Horner
Howard J Federoff
Miriam Gullo
Martin E Schwab
Lorne M Mendell
Victor L Arvanian
Northport VA Medical Center · USGeorgetown University · USStony Brook University · USUniversity of Rochester Medical Center · USUniversity of Washington · US

Funding

MECHANISMS OF PLASTICITY IN NEURONAL CONNECTIONSR01NS016996 · NINDS · STATE UNIVERSITY NEW YORK STONY BROOK · PI MENDELL, LORNE M · 1985 to 2011
$3.9M
NINDS NIH HHS 5R01 NS 16996NINDS NIH HHS R01 NS016996
6 · The paper itself

Abstract

To encourage re-establishment of functional innervation of ipsilateral lumbar motoneurons by descending fibers after an intervening lateral thoracic (T10) hemisection (Hx), we treated adult rats with the following agents: (i) anti-Nogo-A antibodies to neutralize the growth-inhibitor Nogo-A; (ii) neurotrophin-3 (NT-3) via engineered fibroblasts to promote neuron survival and plasticity; and (iii) the NMDA-receptor 2d (NR2d) subunit via an HSV-1 amplicon vector to elevate NMDA receptor function by reversing the Mg(2+) block, thereby enhancing synaptic plasticity and promoting the effects of NT-3. Synaptic responses evoked by stimulation of the ventrolateral funiculus ipsilateral and rostral to the Hx were recorded intracellularly from ipsilateral lumbar motoneurons. In uninjured adult rats short-latency (1.7-ms) monosynaptic responses were observed. After Hx these monosynaptic responses were abolished. In the Nogo-Ab + NT-3 + NR2d group, long-latency (approximately 10 ms), probably polysynaptic, responses were recorded and these were not abolished by re-transection of the spinal cord through the Hx area. This suggests that these novel responses resulted from new connections established around the Hx. Anterograde anatomical tracing from the cervical grey matter ipsilateral to the Hx revealed increased numbers of axons re-crossing the midline below the lesion in the Nogo-Ab + NT-3 + NR2d group. The combined treatment resulted in slightly better motor function in the absence of adverse effects (e.g. pain). Together, these results suggest that the combination treatment with Nogo-Ab + NT-3 + NR2d can produce a functional 'detour' around the lesion in a laterally hemisected spinal cord. This novel combination treatment may help to improve function of the damaged spinal cord.

Indexed as

AnimalsAntibodies, MonoclonalBehavior, AnimalFemaleHumansMotor ActivityMotor NeuronsMyelin ProteinsNeurotrophin 3Nogo ProteinsProtein SubunitsPsychomotor PerformanceRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSpinal CordAntibodies, MonoclonalMyelin ProteinsNeurotrophin 3Nogo ProteinsNR2D NMDA receptorProtein SubunitsReceptors, N-Methyl-D-AspartateRTN4 protein, humanRtn4 protein, rat

Identifiers

PMID21995852
PMCPMC3195885
OpenAlexW1557272041

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.