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Related Experiment Video

Updated: Aug 11, 2025

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Epigenetic function during heroin self-administration controls future relapse-associated behavior in a cell

Ethan M Anderson1, Evgeny Tsvetkov1, Allison Galante1

  • 1Department of Neuroscience, Medical University of South Carolina, Charleston, SC 29425.

Proceedings of the National Academy of Sciences of the United States of America
|February 6, 2023
PubMed
Summary
This summary is machine-generated.

Histone deacetylase 5 (HDAC5) in the nucleus accumbens limits opioid relapse behaviors by regulating gene expression and neuron activity during heroin use. This epigenetic enzyme suppresses drug-seeking behaviors, offering potential therapeutic targets for opioid use disorder (OUD).

Keywords:
epigeneticsexcitabilitynucleus accumbensreinstatement behaviorsubstance use disorder

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Area of Science:

  • Neuroscience
  • Epigenetics
  • Addiction Research

Background:

  • Opioid use creates strong environmental cue associations, increasing relapse risk in individuals with opioid use disorder (OUD).
  • Understanding the epigenetic mechanisms regulating these associations is crucial for developing effective relapse prevention strategies.

Purpose of the Study:

  • To investigate the role of the epigenetic enzyme histone deacetylase 5 (HDAC5) in regulating relapse-associated behaviors in an animal model of OUD.
  • To determine the cell-type-specific functions of HDAC5 within the nucleus accumbens (NAc) in heroin seeking.

Main Methods:

  • Operant self-administration paradigms were used to assess heroin and sucrose seeking.
  • Cre-dependent viral vectors enabled investigation of cell-type-specific HDAC5 effects in dopamine D1 and D2 receptor-expressing medium spiny neurons (MSNs).
  • Cell-type-specific transcriptomics and electrophysiology were employed to analyze gene expression and MSN physiology.

Main Results:

  • NAc HDAC5 expression during heroin self-administration acquisition limited subsequent relapse behaviors.
  • Overexpression of HDAC5 in the NAc suppressed context- and cue-induced heroin seeking, but not sucrose seeking.
  • HDAC5 acted within D1-MSNs to suppress cue-induced seeking and within D2-MSNs to suppress drug-primed seeking.
  • HDAC5 reduced ion transport gene expression and MSN firing rates in both D1- and D2-MSNs.

Conclusions:

  • HDAC5 plays a critical role during active heroin use in limiting distinct relapse triggers by modulating gene expression and MSN activity.
  • These findings suggest HDAC5 as a potential therapeutic target for reducing relapse vulnerability in OUD by regulating ion channel genes and MSN firing rates.