Evidence map›Paper›PMID 30223868›Full record

ArticleMolecular brain2018

Cannabidiol enhances morphine antinociception, diminishes NMDA-mediated seizures and reduces stroke damage via the sigma 1 receptor.

María Rodríguez-Muñoz, Yara Onetti, Elsa Cortés-Montero, Javier Garzón, Pilar Sánchez-Blázquez

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 4% 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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Review of the Interactions Between Anesthetic Agents and Chemotherapeutic Agents in Cancer Cell Lines Studied In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  8. Article
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  10. Article
  11. Article
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  15. Article
  16. Article
  17. CBD in the Treatment of Epilepsy.Molecules (Basel, Switzerland) · 2024
    Review
  18. Article
  19. Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

María Rodríguez-MuñozNeuropharmacology. Department of Traslational Neuroscience, Cajal Institute, CSIC, E-28002, Madrid, Spain.
Yara OnettiNeuropharmacology. Department of Traslational Neuroscience, Cajal Institute, CSIC, E-28002, Madrid, Spain.
Elsa Cortés-MonteroNeuropharmacology. Department of Traslational Neuroscience, Cajal Institute, CSIC, E-28002, Madrid, Spain.
Javier GarzónNeuropharmacology. Department of Traslational Neuroscience, Cajal Institute, CSIC, E-28002, Madrid, Spain.
Pilar Sánchez-BlázquezNeuropharmacology. Department of Traslational Neuroscience, Cajal Institute, CSIC, E-28002, Madrid, Spain. psb@cajal.csic.es.ORCID 0000-0002-7211-4504
Instituto Cajal · ES

Funding

Ministerio de Economía, Industria y Competitividad, Gobierno de España SAF2015-65420-RMinisterio de Sanidad, Servicios Sociales e Igualdad PND2014-012
6 · The paper itself

Abstract

Cannabidiol (CBD), the major non-psychotomimetic compound present in the Cannabis sativa plant, exhibits therapeutic potential for various human diseases, including chronic neurodegenerative diseases, such as Alzheimer's and Parkinson's, ischemic stroke, epilepsy and other convulsive syndromes, neuropsychiatric disorders, neuropathic allodynia and certain types of cancer. CBD does not bind directly to endocannabinoid receptors 1 and 2, and despite research efforts, its specific targets remain to be fully identified. Notably, sigma 1 receptor (σ1R) antagonists inhibit glutamate N-methyl-D-aspartate acid receptor (NMDAR) activity and display positive effects on most of the aforesaid diseases. Thus, we investigated the effects of CBD on three animal models in which NMDAR overactivity plays a critical role: opioid analgesia attenuation, NMDA-induced convulsive syndrome and ischemic stroke. In an in vitro assay, CBD disrupted the regulatory association of σ1R with the NR1 subunit of NMDAR, an effect shared by σ1R antagonists, such as BD1063 and progesterone, and prevented by σ1R agonists, such as 4-IBP, PPCC and PRE084. The in vivo administration of CBD or BD1063 enhanced morphine-evoked supraspinal antinociception, alleviated NMDA-induced convulsive syndrome, and reduced the infarct size caused by permanent unilateral middle cerebral artery occlusion. These positive effects of CBD were reduced by the σ1R agonists PRE084 and PPCC, and absent in σ1R

Indexed as

AnimalsAnticonvulsantsCannabidiolDisease Models, AnimalInfarction, Middle Cerebral ArteryMaleMice, KnockoutMorphineN-MethylaspartateNociceptionProtein SubunitsReceptors, N-Methyl-D-AspartateReceptors, sigmaSeizuresSigma-1 ReceptorStrokeAnticonvulsantsCannabidiolMorphineN-MethylaspartateProtein SubunitsReceptors, N-Methyl-D-AspartateReceptors, sigmaSigma-1 ReceptorAcute painCannabidiolCannabinoidsEpilepsyNeuropathologyNMDA receptorSigma 1 receptorStroke

Identifiers

PMID30223868
PMCPMC6142691
OpenAlexW2890976209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.