Evidence map›Paper›PMID 22075205›Full record

ReviewMolecular and cellular endocrinology2012

Regulation of endocannabinoid release by G proteins: a paracrine mechanism of G protein-coupled receptor action.

Pál Gyombolai, Dorottya Pap, Gábor Turu, Kevin J Catt, György Bagdy, László Hunyady

Open access · greenAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Cannabinoids in the landscape of cancer.Journal of cancer research and clinical oncology · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Activation of the mGluMolecular psychiatry · 2020
    Article
  16. Review
  17. Presynaptic mGluRs Control the Duration of Endocannabinoid-Mediated DSI.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  18. Review
  19. Endocannabinoids in Body Weight Control.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
  20. CBNaunyn-Schmiedeberg's archives of pharmacology · 2017
    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

6 authors at 2 institutions in 2 countries.

Pál GyombolaiDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Dorottya Pap
Gábor Turu
Kevin J Catt
György Bagdy
László Hunyady
Semmelweis University · HUNational Institutes of Health · US

Funding

Regulation of the Hypothalamic GnRH NeuronZIAHD000184 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI CATT, KEVIN J · 2009 to 2012
$5.2M
Intramural NIH HHS ZIA HD000184
6 · The paper itself

Abstract

In the past years, the relationship between the endocannabinoid system (ECS) and other hormonal and neuromodulatory systems has been intensively studied. G protein-coupled receptors (GPCRs) can stimulate endocannabinoid (eCB) production via activation of G(q/11) proteins and, in some cases, G(s) proteins. In this review, we summarize the pathways through which GPCR activation can trigger eCB release, as well as the best known examples of this process throughout the body tissues. Angiotensin II-induced activation of AT(1) receptors, similar to other G(q/11)-coupled receptors, can lead to the formation of 2-arachidonoylglycerol (2-AG), an important eCB. The importance of eCB formation in angiotensin II action is supported by the finding that the hypertensive effect of angiotensin II, injected directly into the hypothalamic paraventricular nucleus of anaesthetized rats, can be abolished by AM251, an inverse agonist of CB(1) cannabinoid receptors (CB(1)Rs). We conclude that activation of the ECS should be considered as a general consequence of the stimulation of G(q/11)-coupled receptors, and may mediate some of the physiological effects of GPCRs.

Indexed as

EndocannabinoidsAngiotensin IIAnimalsArachidonic AcidsCannabinoid Receptor ModulatorsGlyceridesGTP-Binding Protein alpha Subunits, Gq-G11HumansParacrine CommunicationParaventricular Hypothalamic NucleusPiperidinesPyrazolesRatsReceptor, Angiotensin, Type 1Receptor, Cannabinoid, CB1AM 251Angiotensin IIArachidonic AcidsCannabinoid Receptor ModulatorsEndocannabinoidsGlyceridesglyceryl 2-arachidonateGTP-Binding Protein alpha Subunits, Gq-G11PiperidinesPyrazolesReceptor, Angiotensin, Type 1Receptor, Cannabinoid, CB1

Identifiers

PMID22075205
PMCPMC4169275
OpenAlexW2084899934

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.