Evidence map›Paper›PMID 19494156›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Retrograde opioid signaling regulates glutamatergic transmission in the hypothalamus.

Karl J Iremonger, Jaideep S Bains

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

57 citing papers in PubMed, 92 citations in OpenAlex.

  1. Direct Modulation of CRH Nerve Terminal Function by Noradrenaline and Corticosterone.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  2. Article
  3. Review
  4. Substance abuse and neurotransmission.Advances in pharmacology (San Diego, Calif.) · 2022
    Article
  5. Review
  6. Review
  7. Sex-Specific Vasopressin Signaling Buffers Stress-Dependent Synaptic Changes in Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  8. Review
  9. Mu-Opioids Suppress GABAergic Synaptic Transmission onto Orbitofrontal Cortex Pyramidal Neurons with Subregional Selectivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  10. Review
  11. Heterosynaptic GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. GPCR regulation of secretion.Pharmacology & therapeutics · 2018
    Review
  17. Article
  18. Article
  19. Local Corticotropin-Releasing Factor Signaling in the Hypothalamic Paraventricular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  20. 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.

Karl J IremongerHotchkiss Brain Institute and Department of Physiology and Pharmacology, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Jaideep S Bains
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Opioid signaling in the CNS is critical for controlling cellular excitability, yet the conditions under which endogenous opioid peptides are released and the precise mechanisms by which they affect synaptic transmission remain poorly understood. The opioid peptide dynorphin is present in the soma and dendrites of vasopressin neurons in the hypothalamus and dynamically controls the excitability of these cells in vivo. Here, we show that dynorphin is released from dendritic vesicles in response to postsynaptic activity and acts in a retrograde manner to inhibit excitatory synaptic transmission. This inhibition, which requires the activation of kappa-opioid receptors, results from a reduction in presynaptic release of glutamate vesicles. The opioid inhibition is downstream of Ca(2+) entry and is likely mediated by a direct modulation of presynaptic fusion machinery. These findings demonstrate that neurons may self-regulate their excitability through the dendritic release of opioids to inhibit excitatory synaptic transmission.

Indexed as

4-AminopyridineAnalysis of VarianceAnimalsAnimals, Genetically ModifiedAnimals, NewbornBenzeneacetamidesCalciumCalcium Channel BlockersDendritesDynorphinsElectric StimulationEnzyme InhibitorsGlutamic AcidGreen Fluorescent ProteinsInhibitory Postsynaptic PotentialsIn Vitro Techniques4-AminopyridineBenzeneacetamidesCalciumCalcium Channel BlockersDynorphinsEnzyme InhibitorsGlutamic AcidGreen Fluorescent ProteinsNarcotic Antagonistsomega-Conotoxin GVIAPotassium Channel BlockersPyrrolidinesReceptors, OpioidU 69593

Identifiers

PMID19494156
PMCPMC6666467
OpenAlexW2090564875

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.