Evidence map›Paper›PMID 30980832›Full record

ArticleExperimental neurology2019

Depletion of microglia immediately following traumatic brain injury in the pediatric rat: Implications for cellular and behavioral pathology.

Lauren A Hanlon, Ramesh Raghupathi, Jimmy W Huh

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Gut microbes · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. 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 2 institutions in 1 country.

Lauren A HanlonProgram in Neuroscience, Graduate School of Biomedical Sciences and Professional Studies, Drexel University, Philadelphia, PA, United States of America; Department of Neurosurgery, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, United States of America.
Ramesh RaghupathiProgram in Neuroscience, Graduate School of Biomedical Sciences and Professional Studies, Drexel University, Philadelphia, PA, United States of America; Department of Neurobiology and Anatomy, Drexel University, Philadelphia, PA, United States of America. Electronic address: RR79@drexel.edu.
Jimmy W HuhDepartment of Anesthesiology and Critical Care, Children's Hospital of Philadelphia, Philadelphia, PA, United States of America. Electronic address: huh@email.chop.edu.
Drexel University · USChildren's Hospital of Philadelphia · US

Funding

Pathology-directed combination therapy for pediatric TBIR01HD061963 · NICHD · DREXEL UNIVERSITY · PI RAGHUPATHI, RAMESH · 2009 to 2013
$1.4M
Mechanisms of injury and acute repair of axons in TBIR01NS065017 · NINDS · DREXEL UNIVERSITY · PI BARBEE, KENNETH A, GALLO, GIANLUCA · 2010 to 2012
$914k
NICHD NIH HHS R01 HD061963NINDS NIH HHS R01 NS065017
6 · The paper itself

Abstract

The inflammatory response is a significant component of the pathophysiology of pediatric traumatic brain injury. High levels of inflammatory mediators have been found in the cerebrospinal fluid of brain-injured children which have been linked to poor prognosis. Targeting aspects of the inflammatory response in the hopes of finding a viable post-injury therapeutic option has gained attention. Microglia are largely responsible for perpetuating the injury-induced inflammatory response but in the developing brain they play beneficial roles in both normal and disease states. Following closed head injury in the neonate rat, depletion of microglia with intracerebral injections of liposomes containing clodronate was associated with an increase in neurodegeneration in the early post-injury period (3 days) relative to those injected with empty liposomes suggestive of a decrease in clearance of dying cells. In sham-injured animals, microglia repopulated the clodrosome-mediated depleted brain regions over a period of 2-4 weeks and exhibited morphology typical of a resting phenotype. In brain-injured animals, the repopulated microglia in clodrosome-injected animals exhibited rod-like and amoeboid morphologies. However, fluoro-Jade B reactivity in these brain regions was more extensive than in empty liposome-injected animals suggesting that the active microglia may be unable to clear dying neurons. This was accompanied by an induction of hyperexcitability in the local cortical circuitry. Depletion of microglia within the white matter tracts and the thalamus did not affect the extent of injury-induced traumatic axonal injury. Increased neurodegeneration in the dorsal subiculum was not accompanied by any changes to injury-induced deficits in spatial learning and memory. These data suggest that activation of microglia may be important for removal of dying neurons in the traumatically-injured immature brain.

Indexed as

Behavior, AnimalAnalgesics, Non-NarcoticAnimalsAnimals, NewbornBrain Injuries, TraumaticCerebral CortexClodronic AcidFemaleHead Injuries, ClosedMaleMaze LearningMemoryMicrogliaNerve DegenerationNeuronsPsychomotor PerformanceAnalgesics, Non-NarcoticClodronic AcidClodronateCortical activityMicrogliaNeurodegenerationPediatric TBISpatial learning

Identifiers

PMID30980832
PMCPMC6544393
OpenAlexW2939809860

What OpenQuestion holds

Textmetadata
LicenceTDM
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.