Evidence map›Paper›PMID 22946098›Full record

ArticleThe Journal of physiology2012

Endocannabinoids mediate the glucocorticoid-induced inhibition of excitatory synaptic transmission to dorsal raphe serotonin neurons.

Jue Wang, Roh-Yu Shen, Samir Haj-Dahmane

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Neurobiological Interactions Between Stress and the Endocannabinoid System.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Review
  13. A peripheral endocannabinoid mechanism contributes to glucocorticoid-mediated metabolic syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  14. Chronic stress impairs α1-adrenoceptor-induced endocannabinoid-dependent synaptic plasticity in the dorsal raphe nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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

3 authors at 1 institution in 1 country.

Jue WangResearch Institute on Addictions, University at Buffalo, 1021 Main Street, Buffalo, NY 14203, USA.
Roh-Yu Shen
Samir Haj-Dahmane
University at Buffalo, State University of New York · US

Funding

Stress and Endocannabinoids in Serotonin NeuronsR01MH078009 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI HAJ-DAHMANE, SAMIR · 2007 to 2011
$1.6M
NIMH NIH HHS MH078009NIMH NIH HHS R01 MH078009
6 · The paper itself

Abstract

Glucocorticoids play a critical role in the modulation of stress responses by controlling the function of the serotonin (5-HT) system. However, the precise effects of glucocorticoids on the excitability of dorsal raphe (DR) 5-HT neurons remain unknown. In this study, we investigated the effects of glucocorticoids on excitatory synaptic transmission to putative DR 5-HT neurons. We found that corticosterone or the synthetic glucocorticoid agonist dexamethasone rapidly suppressed glutamatergic synaptic transmission to DR 5-HT neurons by inhibiting glutamate release in the DR. This inhibitory effect was mimicked by membrane-impermeable glucocorticoids, indicating the involvement of membrane-located corticosteroid receptors. The glucocorticoid-induced inhibition of glutamatergic transmission was mediated by the activation of postsynaptic G-protein-coupled receptors and signalled by retrograde endocannabinoid (eCB) messengers. Examination of the downstream mechanisms revealed that glucocorticoids enhance eCB signalling via an inhibition of cyclooxygenase-2. Together, these findings unravel a novel mechanism by which glucocorticoids control the excitability of DR 5-HT neurons and provide new insight into the rapid effects of stress hormones on the function of the 5-HT system.

Indexed as

AnimalsCorticosteroneCyclooxygenase 2 InhibitorsDexamethasoneEndocannabinoidsExcitatory Postsynaptic PotentialsGlucocorticoidsGlutamic AcidMaleRaphe NucleiRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledSerotonergic NeuronsSignal TransductionCorticosteroneCyclooxygenase 2 InhibitorsDexamethasoneEndocannabinoidsGlucocorticoidsGlutamic AcidReceptors, G-Protein-Coupled

Identifiers

PMID22946098
PMCPMC3528992
OpenAlexW2139688864

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.