Evidence map›Paper›PMID 17220914›Full record

ArticleBritish journal of pharmacology2007

Control of spasticity in a multiple sclerosis model is mediated by CB1, not CB2, cannabinoid receptors.

G Pryce, D Baker

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
7.4field-weighted citation impact, top 3% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 126 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Smoked cannabis for spasticity in multiple sclerosis: a randomized, placebo-controlled trial.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2012
    Trial
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Botanically-Derived ΔMolecules (Basel, Switzerland) · 2022
    Article
  10. Review
  11. The CBCannabis and cannabinoid research · 2021
    Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. WWL70 attenuates PGEJournal of neuroinflammation · 2017
    Article
  17. Review
  18. Review
  19. Neuroprotection in Experimental Autoimmune Encephalomyelitis and Progressive Multiple Sclerosis by Cannabis-Based Cannabinoids.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015
    Review
  20. Turning Over a New Leaf: Cannabinoid and Endocannabinoid Modulation of Immune Function.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015
    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

2 authors at 1 institution in 1 country.

G PryceDepartment of Neuroinflammation, Institute of Neurology, University College London, London, UK.
D Baker
University College London · GB

Funding

Multiple Sclerosis Society 541Multiple Sclerosis Society 835
6 · The paper itself

Abstract

background and purposeThere is increasing evidence to suggest that cannabis can ameliorate muscle-spasticity in multiple sclerosis, as was objectively shown in experimental autoimmune encephalomyelitis models. The purpose of this study was to investigate further the involvement of CB1 and CB2)cannabinoid receptors in the control of experimental spasticity. EXPERIMENTAL APPROACH: Spasticity was induced in wildtype and CB1-deficient mice following the development of relapsing, experimental autoimmune encephalomyelitis. Spastic-hindlimb stiffness was measured by the resistance to flexion against a strain gauge following the administration of CB1 and CB2 agonists. KEY

resultsAs previously suggested, some CB2-selective agonists (RWJ400065) could inhibit spasticity. Importantly, however, the anti-spastic activity of RWJ400065 and the therapeutic effect of non-selective CB1/CB2 agonists (R(+)WIN55,212-2 and CP55, 940) was lost in spastic, CB1-deficit mice. CONCLUSIONS AND IMPLICATIONS: The CB1 receptor controls spasticity and cross-reactivity to this receptor appears to account for the therapeutic action of some CB2 agonists. As cannabinoid-induced psychoactivity is also mediated by the CB1 receptor, it will be difficult to truly dissociate the therapeutic effects from the well-known, adverse effects of cannabinoids when using cannabis as a medicine. The lack of knowledge on the true diversity of the cannabinoid system coupled with the lack of total specificity of current cannabinoid reagents makes interpretation of in vivo results difficult, if using a purely pharmacological approach. Gene knockout technology provides an important tool in target validation and indicates that the CB1 receptor is the main cannabinoid target for an anti-spastic effect.

Indexed as

AnimalsBenzoxazinesBody TemperatureCross ReactionsCyclohexanolsEncephalomyelitis, Autoimmune, ExperimentalMiceMice, KnockoutMorpholinesMultiple SclerosisMuscle SpasticityNaphthalenesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB23-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanoneBenzoxazinesCyclohexanolsMorpholinesNaphthalenesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2

Identifiers

PMID17220914
PMCPMC2189718
OpenAlexW1559076309

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.