Evidence map›Paper›PMID 31793909›Full record

ArticleThe Journal of clinical investigation2020

Gabapentinoid treatment promotes corticospinal plasticity and regeneration following murine spinal cord injury.

Wenjing Sun, Molly Je Larson, Conrad M Kiyoshi, Alexander J Annett, William A Stalker, Juan Peng, Andrea Tedeschi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

39 citing papers in PubMed, 68 citations in OpenAlex.

  1. Gabapentin and cognitive impairment after traumatic brain injury: A multinational cohort of 49,925 patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Article
  3. Article
  4. Repurposing of Chemokine Antagonists for Combined Phase-Resolved Spinal Cord Injury Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  5. Review
  6. Article
  7. Review
  8. Synaptotagmin 4 Supports Spontaneous Axon Sprouting after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Observational
  19. Review
  20. Gabapentin-Friend or foe?Pain practice : the official journal of World Institute of Pain · 2023
    Review
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

7 authors at 2 institutions in 2 countries.

Wenjing SunDepartment of Neuroscience, Wexner Medical Center.
Molly Je LarsonDepartment of Neuroscience, Wexner Medical Center.
Conrad M KiyoshiDepartment of Neuroscience, Wexner Medical Center.
Alexander J AnnettDepartment of Neuroscience, Wexner Medical Center.
William A StalkerDepartment of Neuroscience, Wexner Medical Center.
Juan PengCenter for Biostatistics and Bioinformatics, and.
Andrea TedeschiDepartment of Neuroscience, Wexner Medical Center.
The Ohio State University Wexner Medical Center · USInstitute for Medical Informatics and Biostatistics · CH

Funding

Ohio State University Neuroscience Center Core-Core EP30NS104177 · NINDS · OHIO STATE UNIVERSITY · PI BROWN, ANTHONY · 2017 to 2020
$1.9M
Targeting Non-Neuronal Mechanisms for Spinal Cord Injury RepairR01NS110681 · NINDS · OHIO STATE UNIVERSITY · PI TEDESCHI, ANDREA · 2019 to 2023
$1.7M
Cellular and molecular mechanisms of maladaptive homeostatic plasticity and chronic neurodegenerationR21NS109787 · NINDS · OHIO STATE UNIVERSITY · PI TEDESCHI, ANDREA · 2019 to 2019
$409k
NINDS NIH HHS P30 NS104177NINDS NIH HHS R01 NS110681NINDS NIH HHS R21 NS109787
6 · The paper itself

Abstract

Axon regeneration failure causes neurological deficits and long-term disability after spinal cord injury (SCI). Here, we found that the α2δ2 subunit of voltage-gated calcium channels negatively regulates axon growth and regeneration of corticospinal neurons, the cells that originate the corticospinal tract. Increased α2δ2 expression in corticospinal neurons contributed to loss of corticospinal regrowth ability during postnatal development and after SCI. In contrast, α2δ2 pharmacological blockade through gabapentin administration promoted corticospinal structural plasticity and regeneration in adulthood. Using an optogenetic strategy combined with in vivo electrophysiological recording, we demonstrated that regenerating corticospinal axons functionally integrate into spinal circuits. Mice administered gabapentin recovered upper extremity function after cervical SCI. Importantly, such recovery relies on reorganization of the corticospinal pathway, as chemogenetic silencing of injured corticospinal neurons transiently abrogated recovery. Thus, targeting α2δ2 with a clinically relevant treatment strategy aids repair of motor circuits after SCI.

Indexed as

AnimalsAxonsDisease Models, AnimalFemaleGabapentinMaleMiceMice, TransgenicNerve RegenerationReceptors, NicotinicSpinal InjuriesGabapentinReceptors, NicotinicMouse modelsNeurological disordersNeuroscience

Identifiers

PMID31793909
PMCPMC6934190
OpenAlexW2992154409

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.