CoChat
Sign Up
Cited by 379Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchBarrier Structure and Function Studies

Inflammatory leukocytic recruitment and diffuse neuronal degeneration are separate pathological processes resulting from traumatic brain injury

Open access
Soares, HD, Hicks, RR, Smith, D, McIntosh, TK·1995·The Journal of Neuroscience
DOI 10.1523/jneurosci.15-12-08223.1995PMC PMC6577921
Open this paper in CoChat — free accountOpen PDF

Abstract

The present study characterized whether inflammatory leukocytic infiltration is temporally and regionally correlated with neuronal degeneration and/or blood brain barrier (BBB) breakdown resulting from traumatic brain injury. Adult rats were sacrificed at 5 min, 2, 4, 12, 24, and 72 hr after lateral fluid percussion brain injury. BBB breakdown, neuronal degeneration and leukocyte infiltration were assessed using immunocytochemistry, silver impregnation and toluidine blue and eosin staining. BBB breakdown and neuronal degeneration occurred concomitantly in injured cortex, hippocampus, and along the dorsolateral quadrant of the diencephalon. However, neuronal degeneration within deep diencephalic structures transpired in the absence of IgG extravasation. Neutrophils were observed only in regions exhibiting BBB damage and were first apparent in injured cortex and hippocampus between 2–12 hr posttrauma lining the vasculature and filling subarachnoid/subdural spaces. Neutrophils then migrated from damaged vasculature into traumatized cortical and hippocampal parenchyma by 24 hr after lateral fluid percussion injury. Macrophages were also observed within cortical parenchyma at 24 hr and completely filled the cortical lesion site by 72 hr after injury. Macrophages were not as abundant throughout hippocampal parenchyma and were found only in hippocampal regions exhibiting focal hemorrhage at 72 hr. Finally, neutrophils did not migrate to deep diencephalic structures that showed no BBB damage despite extensive neuronal degeneration. Indeed, lateral fluid percussion elicits inflammatory leukocytic recruitment only in regions experiencing concomitant BBB damage and neuronal degeneration. In summary, inflammatory leukocytic recruitment and diffuse neuronal degeneration are separate pathological processes resulting from traumatic brain injury.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1523/jneurosci.15-12-08223.1995

Cites

70 of 70 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Excessive or chronic neuroinflammation is linked to progressive changes, including atrophy, neuronal loss, and axonal degeneration.

    “Excessive or chronic neuroinflammation is linked to progressive changes, including atrophy, neuronal loss, and axonal degeneration (84, 103–105).”

    From The Inflammatory Continuum of Traumatic Brain Injury and Alzheimer’s Disease (2018) · cites this paper as [104]

    The discussion (page unavailable) reports both inflammatory recruitment and neuronal degeneration after traumatic brain injury, but says diffuse diencephalic degeneration can occur without leukocyte infiltration and describes the processes as distinct. The study follows rats for up to 72 hours; it does not establish a link between excessive or chronic neuroinflammation and progressive atrophy or axonal degeneration. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • TBI is a biphasic injury: after the mechanical primary injury, a secondary dystrophic state produces long-term dysfunction including elevated neuroinflammation due to blood-brain barrier disruption, increased oxidative stress, and persistent changes in the microglial population.

    “TBI is a biphasic injury: after the mechanical primary injury, a secondary dystrophic state produces long-term dysfunction in the brain that includes elevated neuroinflammation as a result of blood-brain barrier disruption, increased oxidative stress, and persistent changes in the microglial population [100–106].”

    From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [103]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Kochanek PM, Nemoto EM, Evans RW, Schoettle RJ (1990) Poly- morphonuclear leukocytes, platelets, and lipid mediators in the patho- genesis of ischemic and traumatic central nervous system injury. In: Lipid mediators in ischemic brain damage and experimental epilep- sy-new trends in lipid mediators research (Bazan NG, ed), pp 220- 240. Basel: Karger.

Cited by

Sorted by citations

Related

Authors
Soares, H., Hicks, R., Smith, D., & McIntosh, T.
Affiliations
St. Jude Children's Research Hospital (US)
ORCID
Smith, D
Venue
The Journal of Neuroscience
Publisher
Society for Neuroscience
Published
1995-12-01
Volume
15
Issue
12
Pages
8223-8233
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
DOI
10.1523/jneurosci.15-12-08223.1995
PMC
PMC6577921
OpenAlex
W1666499734
Cited by
379
References
70
Citations by year
2026: 1 · 2025: 2 · 2024: 13 · 2023: 2 · 2022: 11 · 2021: 18 · 2020: 15 · 2019: 18 · 2018: 9 · 2017: 13 · 2016: 14 · 2015: 11 · 2014: 12 · 2013: 20 · 2012: 19
FWCI
10.37
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (NS08803, NS26818)
  • National Institute of Neurological Disorders and Stroke (NS-08803, NS26818)
Topics
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
Keywords
traumatic brain injury, leukocyte recruitment, neutrophils, macrophages, blood-brain barrier disruption, neurodegeneration, lateral fluid percussion injury, hippocampus, cerebral cortex, diencephalon, IgG extravasation, neuroinflammation
MeSH terms
Animals, Blood-Brain Barrier, Brain, Brain Concussion, Brain Injuries, Encephalitis, Immunoglobulin G, Leukocytes, Male, Neurons, Time Factors, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review