Evidence map›Paper›PMID 30049887›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Transneuronal Downregulation of the Premotor Cholinergic System After Corticospinal Tract Loss.

Yu-Qiu Jiang, Adrish Sarkar, Alzahraa Amer, John H Martin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. C-Boutons and Their Influence on Amyotrophic Lateral Sclerosis Disease Progression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  6. Article
  7. Review
  8. Maturation of the Locomotor Circuitry in Children With Cerebral Palsy.Frontiers in bioengineering and biotechnology · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. 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

4 authors at 2 institutions in 1 country.

Yu-Qiu JiangDepartment of Molecular, Cellular, and Biomedical Sciences, City University of New York School of Medicine at City College, New York, New York 10031 and.ORCID 0000-0002-0691-1329
Adrish SarkarDepartment of Molecular, Cellular, and Biomedical Sciences, City University of New York School of Medicine at City College, New York, New York 10031 and.ORCID 0000-0002-9251-4310
Alzahraa AmerDepartment of Molecular, Cellular, and Biomedical Sciences, City University of New York School of Medicine at City College, New York, New York 10031 and.ORCID 0000-0003-4729-1186
John H MartinDepartment of Molecular, Cellular, and Biomedical Sciences, City University of New York School of Medicine at City College, New York, New York 10031 and jmartin@ccny.cuny.edu.ORCID 0000-0002-8670-8469
City College of New York · USThe Graduate Center, CUNY · US

Funding

Cellular/Molecular Basis of Development: Research CenterG12MD007603 · NIMHD · CITY COLLEGE OF NEW YORK · PI PEZZANO, MARK · 2012 to 2017
$11.5M
Lesion and Activity Dependent Corticospinal Tract PlasticityR01NS064004 · NINDS · RESEARCH FOUNDATION OF THE CITY UNIVERSITY OF NEW YORK D/B/A RF CUNY - CUNY SCHOOL OF MEDICINE · PI John H Martin · 2009 to 2026
$5.2M
NIMHD NIH HHS G12 MD007603NINDS NIH HHS R01 NS064004
6 · The paper itself

Abstract

Injury to the supraspinal motor systems, especially the corticospinal tract, leads to movement impairments. In addition to direct disruption of descending motor pathways, spinal motor circuits that are distant to and not directly damaged by the lesion undergo remodeling that contributes significantly to the impairments. Knowing which spinal circuits are remodeled and the underlying mechanisms are critical for understanding the functional changes in the motor pathway and for developing repair strategies. Here, we target spinal premotor cholinergic interneurons (IN) that directly modulate motoneuron excitability via their cholinergic C-bouton terminals. Using a model of unilateral medullary corticospinal tract lesion in male rats, we found transneuronal downregulation of the premotor cholinergic pathway. Phagocytic microglial cells were upregulated in parallel with cholinergic pathway downregulation and both were blocked by minocycline, a microglia activation inhibitor. Additionally, we found a transient increase in interneuronal complement protein C1q expression that preceded cell loss. 3D reconstructions showed ongoing phagocytosis of C1q-expressing cholinergic INs by microglia 3 d after injury, which was complete by 10 d after injury. Unilateral motor cortex inactivation using the GABA

Indexed as

AnimalsCervical CordCholinergic NeuronsComplement C1qInterneuronsMaleMicrogliaMotor CortexMotor NeuronsNeuronal PlasticityPhagocytosisPyramidal TractsRats, Sprague-DawleySpinal Cord StimulationComplement C1qactivity dependencecholinergic interneuroncomplement protein C1qcorticospinal tractphagocytic microglia

Identifiers

PMID30049887
PMCPMC6158693
OpenAlexW2884002081

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.