Evidence map›Paper›PMID 31391209›Full record

ArticleThe Journal of experimental medicine2019

Corticospinal circuit remodeling after central nervous system injury is dependent on neuronal activity.

Peter M Bradley, Carmen K Denecke, Almir Aljovic, Anja Schmalz, Martin Kerschensteiner, Florence M Bareyre

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Review
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  4. Review
  5. Article
  6. Article
  7. Chronic Adaptations in the Dorsal Horn Following a Cervical Spinal Cord Injury in Primates.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Motoneuron-Specific PTEN Deletion in Mice Induces Neuronal Hypertrophy and Also Regeneration after Facial Nerve Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Review
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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

6 authors.

Peter M Bradley *Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
Carmen K Denecke *Institute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
Almir AljovicInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.ORCID 0000-0001-9725-6368
Anja SchmalzInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
Martin KerschensteinerInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
Florence M BareyreInstitute of Clinical Neuroimmunology, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany florence.bareyre@med.uni-muenchen.de.ORCID 0000-0002-0917-1725

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The remodeling of supraspinal axonal circuits mediates functional recovery after spinal cord injury. This process critically depends on the selection of appropriate synaptic connections between cortical projection and spinal relay neurons. To unravel the principles that guide this target selection, we used genetic and chemogenetic tools to modulate NMDA receptor (NMDAR) integrity and function, CREB-mediated transcription, and neuronal firing of relay neurons during injury-induced corticospinal remodeling. We show that NMDAR signaling and CREB-mediated transcription maintain nascent corticospinal tract (CST)-relay neuron contacts. These activity-dependent signals act during a defined period of circuit remodeling and do not affect mature or uninjured circuits. Furthermore, chemogenetic modulation of relay neuron activity reveals that the regrowing CST axons select their postsynaptic partners in a competitive manner and that preventing such activity-dependent shaping of corticospinal circuits limits motor recovery after spinal cord injury.

Indexed as

AnimalsAxonsCentral Nervous SystemCyclic AMP Response Element-Binding ProteinFemaleMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicModels, NeurologicalNerve RegenerationNeuronsPyramidal TractsReceptors, N-Methyl-D-AspartateRecovery of FunctionSpinal Cord InjuriesCreb1 protein, mouseCyclic AMP Response Element-Binding ProteinNR1 NMDA receptorReceptors, N-Methyl-D-Aspartate

Identifiers

PMID31391209
PMCPMC6829605

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.