Evidence map›Paper›PMID 20720126›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Repeated stress impairs endocannabinoid signaling in the paraventricular nucleus of the hypothalamus.

Jaclyn I Wamsteeker, J Brent Kuzmiski, Jaideep S Bains

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 2% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Glucocorticoid-endocannabinoid crosstalk in the ventrolateral periaqueductal gray (vlPAG) promotes pain resolution.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  9. Inflammation and cancer: friend or foe?Frontiers in pharmacology · 2024
    Review
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  11. Review
  12. 2-AG-Mediated Control of GABAergic Signaling Is Impaired in a Model of Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  13. Endocannabinoids at the synapse and beyond: implications for neuropsychiatric disease pathophysiology and treatment.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  14. Multiplexed Membrane Signaling by Glucocorticoids.Current opinion in endocrine and metabolic research · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

4 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

3 authors at 1 institution in 1 country.

Jaclyn I WamsteekerHotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
J Brent Kuzmiski
Jaideep S Bains
University of Calgary · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Endocannabinoids (eCBs) are ubiquitous retrograde signaling molecules in the nervous system that are recruited in response to robust neuronal activity or the activation of postsynaptic G-protein-coupled receptors. Physiologically, eCBs have been implicated as important mediators of the stress axis and they may contribute to the rapid feedback inhibition of the hypothalamic-pituitary-adrenal axis (HPA) by circulating corticosteroids (CORTs). Understanding the relationship between stress and eCBs, however, is complicated by observations that eCB signaling is itself sensitive to stress. The mechanisms that link stress to changes in synaptic eCB signaling and the impact of these changes on CORT-mediated negative feedback have not been resolved. Here, we show that repetitive immobilization stress, in juvenile male rats, causes a functional downregulation of CB(1) receptors in the paraventricular nucleus of the hypothalamus (PVN). This loss of CB(1) receptor signaling, which requires the activation of genomic glucocorticoid receptors, impairs both activity and receptor-dependent eCB signaling at GABA and glutamate synapses on parvocellular neuroendocrine cells in PVN. Our results provide a plausible mechanism for how stress can lead to alterations in CORT-mediated negative feedback and may contribute to the development of plasticity of HPA responses.

Indexed as

EndocannabinoidsSignal TransductionAnimalsCannabinoid Receptor ModulatorsChronic Diseasegamma-Aminobutyric AcidHippocampusInhibitory Postsynaptic PotentialsIn Vitro TechniquesMaleNeural InhibitionNeuroendocrine CellsNeuronsParaventricular Hypothalamic NucleusPresynaptic TerminalsRatsCannabinoid Receptor ModulatorsEndocannabinoidsgamma-Aminobutyric AcidReceptor, Cannabinoid, CB1Receptors, G-Protein-Coupled

Identifiers

PMID20720126
PMCPMC6633493
OpenAlexW2003823489

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.