Evidence map›Paper›PMID 20832403›Full record

ArticleExperimental neurology2010

A synthetic cannabinoid agonist promotes oligodendrogliogenesis during viral encephalitis in rats.

Marylou V Solbrig, Yijun Fan, Neal Hermanowicz, Maria Grazia Morgese, Andrea Giuffrida

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
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  4. Article
  5. Article
  6. Review
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  8. Article
  9. Review
  10. Cannabinoids and glial cells: possible mechanism to understand schizophrenia.European archives of psychiatry and clinical neuroscience · 2018
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. PET imaging in multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014
    Review
  16. Article
  17. Review
  18. Article
  19. New insights on endocannabinoid transmission in psychomotor disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2012
    Review
  20. 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

5 authors at 4 institutions in 3 countries.

Marylou V SolbrigDepartment of Medicine (Neurology), University of Manitoba, Winnipeg, Manitoba, Canada. msolbrig2@hsc.mb.ca
Yijun Fan
Neal Hermanowicz
Maria Grazia Morgese
Andrea Giuffrida
University of Manitoba · CAThe University of Texas Health Science Center at San Antonio · USUniversity of California, Irvine · USUniversity of Foggia · IT

Funding

Role of Endocannabinoids in Levodopa-Induced DyskinesiasR01NS050401 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI GIUFFRIDA, ANDREA · 2005 to 2012
$2.3M
Viral neuropathology neuropeptides and epilepsyR01NS042307 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI SOLBRIG, MARYLOU V · 2003 to 2005
$1.1M
NINDS NIH HHS NS 042307NINDS NIH HHS NS 050401-06NINDS NIH HHS R01 NS042307NINDS NIH HHS R01 NS050401
6 · The paper itself

Abstract

Chronic CNS infection by several families of viruses can produce deficits in prefrontal cortex (PFC) and striatal function. Cannabinoid drugs have been long known for their anti-inflammatory properties and their ability to modulate adult neuro and gliogenesis. Therefore, we explored the effects of systemic administration of the cannabinoid agonist WIN55,212-2(WIN) on prefrontal cortex (PFC) and striatal cytogenesis in a viral model of CNS injury and inflammation based on Borna Disease (BD) virus encephalitis. Active BrdU(+) progenitor populations were significantly decreased 1 week after BrdU labeling in BD rats [p<0.001 compared to uninfected (NL) controls] while less than 5% of BrdU(+) cells colabeled for BDV protein. Systemic WIN (1mg/kg i.p. twice daily×7 days) increased the survival of BrdU(+) cells in striatum (p<0.001) and PFC of BD rats, with differential regulation of labeled oligodendroglia precursors vs microglia/macrophages. WIN increased the percentage of BrdU(+) oligodendrocyte precursor cells and decreased BrdU(+) ED-1-labeled phagocytic cells, without producing pro- or antiviral effects. BDV infection decreased the levels of the endocannabinoid anandamide (AEA) in striatum (p<0.05 compared to NL rats), whereas 2-AG levels were unchanged. Our findings indicate that: 1) viral infection is accompanied by alterations of AEA transmission in the striatum, but new cell protection by WIN appears independent of its effect on endocannabinoid levels; and 2) chronic WIN treatment alters the gliogenic cascades associated with CNS injury, promoting oligodendrocyte survival. Limiting reactive gliogenesis and macrophage activity in favor of oliogodendroglia development has significance for demyelinating diseases. Moreover, the ability of cannabinoids to promote the development of biologically supportive or symbiotic oligodendroglia may generalize to other microglia-driven neurodegenerative syndromes including NeuroAIDS and diseases of aging.

Indexed as

AnimalsAntimetabolitesBenzoxazinesBorna disease virusBromodeoxyuridineCannabinoid Receptor ModulatorsCannabinoidsCell CountCell DifferentiationCell SurvivalEncephalitis, ViralImage Processing, Computer-AssistedImmunohistochemistryMacrophagesMaleMorpholines(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanoneAntimetabolitesBenzoxazinesBromodeoxyuridineCannabinoid Receptor ModulatorsCannabinoidsMorpholinesNaphthalenes

Identifiers

PMID20832403
PMCPMC2981070
OpenAlexW2089504919

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.