Evidence map›Paper›PMID 25288139›Full record

ArticleMolecular psychiatry2015

Epigenetic modulation of chronic anxiety and pain by histone deacetylation.

L Tran, J Schulkin, C O Ligon, B Greenwood-Van Meerveld

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.5field-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

47 citing papers in PubMed, 148 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. The role of epigenetics in anxiety disorders.Molecular biology reports · 2023
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Abdominal and Pelvic Pain: Current Challenges and Future Opportunities.Frontiers in pain research (Lausanne, Switzerland) · 2021
    Article
  17. Article
  18. NADSignal transduction and targeted therapy · 2020
    Review
  19. Article
  20. Review
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

4 authors at 2 institutions in 1 country.

L TranOklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
J SchulkinDepartment of Neuroscience, Georgetown University, Washington, DC, USA.
C O LigonOklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
B Greenwood-Van MeerveldOklahoma Center for Neuroscience, University of Oklahoma Health Science Center, Oklahoma City, OK, USA.
University of Oklahoma Health Sciences Center · USGeorgetown University · US

Funding

Central Mechanisms Modulating Visceral SensitivityI01BX002188 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI HOUCHEN, COURTNEY WAYNE · 2013 to 2022
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BLRD VA I01 BX002188
6 · The paper itself

Abstract

Prolonged exposure of the central amygdala (CeA) to elevated corticosteroids (CORT) facilitates long-term anxiety and pain through activation of glucocorticoid receptors (GRs) and corticotropin-releasing factor (CRF). However, the mechanisms maintaining these responses are unknown. Since chronic phenotypes can be sustained by epigenetic mechanisms, including histone modifications such as deacetylation, we tested the hypothesis that histone deacetylation contributes to the maintenance of chronic anxiety and pain induced by prolonged exposure of the CeA to CORT. We found that bilateral infusions of a histone deacetylase inhibitor into the CeA attenuated anxiety-like behavior as well as somatic and visceral hypersensitivity resulting from elevated CORT exposure. Moreover, we delineated a novel pathway through which histone deacetylation could contribute to CORT regulation of GR and subsequent CRF expression in the CeA. Specifically, deacetylation of histone 3 at lysine 9 (H3K9), through the coordinated action of the NAD+-dependent protein deacetylase sirtuin-6 (SIRT6) and nuclear factor kappa B (NFκB), sequesters GR expression leading to disinhibition of CRF. Our results indicate that epigenetic programming in the amygdala, specifically histone modifications, is important in the maintenance of chronic anxiety and pain.

Indexed as

Adrenal Cortex HormonesAnimalsAnxiety DisordersBehavior, AnimalCentral Amygdaloid NucleusCorticotropin-Releasing HormoneDisease Models, AnimalEpigenomicsHistone DeacetylasesHistonesMaleNF-kappa B p50 SubunitPainRatsRats, Inbred F344Receptors, GlucocorticoidAdrenal Cortex HormonesCorticotropin-Releasing HormoneHistone DeacetylasesHistonesNF-kappa B p50 SubunitReceptors, Glucocorticoidsirtuin 6, ratSirtuins

Identifiers

PMID25288139
OpenAlexW2074409078

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.