RNA-Seq Analysis of Morphine-Induced Gene Expression Changes in the Mouse Nucleus Accumbens
Seyed Mahmoud Pourmand1, Shahrzad Nazari2, Elham Nazari3
1Department of Addiction, Tehran Institute of Psychiatry, School of Behavioral Sciences and Mental Health, Iran University of Medical Sciences, Tehran, Iran.
Iranian Journal of Pharmaceutical Research : IJPR
|July 22, 2026
Summary
Chronic morphine exposure alters gene expression in the mouse nucleus accumbens, impacting synaptic plasticity and neurogenesis. This study identifies key genes like NMDA receptor subunits and FGF3 as potential therapeutic targets for opioid use disorder (OUD).
Area of Science:
- Neuroscience
- Genomics
- Bioinformatics
Background:
- Opioid use disorder (OUD) is a major global health issue.
- The nucleus accumbens (NAc) is crucial for reward processing and opioid-induced adaptations.
- Understanding gene expression in the NAc is key to addiction research.
Purpose of the Study:
- To analyze transcriptomic changes in the NAc after chronic morphine exposure in mice.
- To identify molecular mechanisms underlying addiction using RNA sequencing and bioinformatics.
Main Methods:
- RNA sequencing (RNA-Seq) of NAc from morphine- and saline-treated mice.
- Differential gene expression analysis using DESeq2.
- Gene Ontology (GO), KEGG, and protein-protein interaction (PPI) network analyses.
Main Results:
- Distinct transcriptomic profiles were observed between morphine and control groups.
- 143 differentially expressed genes (DEGs) were identified (125 up-regulated, 18 down-regulated).
- Key pathways involved synaptic signaling, ion transport, and neurodegeneration. Hub genes include FGF3, MKI67, GRIN2A/B, GLI1, and AGO2.
Conclusions:
- Chronic morphine alters NAc gene expression, affecting synaptic remodeling and neuroplasticity related to addiction.
- Identified candidate therapeutic targets include NMDA receptor subunits, FGF3, and AGO2.
- Further research is needed to validate these targets for OUD treatment.
