Evidence map›Paper›PMID 23273833›Full record

ArticleThe journal of pain2013

Epigenetic regulation of opioid-induced hyperalgesia, dependence, and tolerance in mice.

De-Yong Liang, XiangQi Li, J David Clark

Open access · bronzeAbstract read
In one paragraph

Article in The journal of pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

54 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
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  6. Article
  7. Role of HDAC5 Epigenetics in Chronic Craniofacial Neuropathic Pain.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Epigenetic Modulation of Opioid Receptors by Drugs of Abuse.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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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.

De-Yong LiangDepartment of Anesthesiology, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA. dyliang@stanford.edu
XiangQi Li
J David Clark
VA Palo Alto Health Care System · US

Funding

Genetic Determinants of Opioid-Induced HyperalgesiaR01DA021332 · NIDA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI CLARK, DAVID J. · 2007 to 2011
$1.2M
NIDA NIH HHS R01 DA021332
6 · The paper itself

Abstract

unlabelledRepeated administration of opioids such as morphine induces persistent behavioral changes including opioid-induced hyperalgesia (OIH), tolerance, and physical dependence. In the current work we explored how the balance of histone acetyltransferase (HAT) versus histone deacetylase (HDAC) might regulate these morphine-induced changes. Nociceptive thresholds, analgesia, and physical dependence were assessed during and for a period of several weeks after morphine exposure. To probe the roles of histone acetylation, the HAT inhibitor curcumin or a selective HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) was administered daily to groups of animals. Histone acetylation in spinal cord was assessed by Western blot and immunohistochemistry. Concurrent administration of curcumin with morphine for 4 days significantly reduced development of opioid-induced mechanical allodynia, thermal hyperalgesia, tolerance, and physical dependence. Conversely, the HDAC inhibitor SAHA enhanced these responses. Interestingly, SAHA treatment after the termination of opioid administration sustained these behavioral changes for at least 4 weeks. Histone H3 acetylation in the dorsal horn of the spinal cord was increased after chronic morphine treatment, but H4 acetylation was unchanged. Moreover, we observed a decrease in HDAC activity in the spinal cords of morphine-treated mice while overall HAT activity was unchanged, suggesting a shift toward a state of enhanced histone acetylation. PERSPECTIVE: The current study indicates that epigenetic mechanisms play a crucial role in opioid-induced long-lasting neuroplasticity. These results provide new sight into understanding the mechanisms of opioid-induced neuroplasticity and suggest new strategies to limit opioid abuse potential and increase the value of these drugs as analgesics.

Indexed as

Epigenesis, GeneticAnalgesics, OpioidAnimalsAnti-Inflammatory Agents, Non-SteroidalBehavior, AnimalBlotting, WesternBrain-Derived Neurotrophic FactorChromatin ImmunoprecipitationCurcuminDose-Response Relationship, DrugDrug ToleranceHistone Deacetylase InhibitorsHot TemperatureHydroxamic AcidsHyperalgesiaMaleAnalgesics, OpioidAnti-Inflammatory Agents, Non-SteroidalBrain-Derived Neurotrophic FactorCurcuminHistone Deacetylase InhibitorsHydroxamic AcidsMorphineVorinostat

Identifiers

PMID23273833
PMCPMC3539745
OpenAlexW2016463798

What OpenQuestion holds

Textmetadata
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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.