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Nucleus Accumbens Hyperactivity and mPFC-NAc Circuit Dysfunction Promote Self-Injurious Behavior in Rats
Yanmei Chen1, Zhonghui Zuo1, Di Luo1,2
1Department of Basic Medicine, Medical School, Kunming University of Science and Technology, Kunming 650550, China.
International Journal of Molecular Sciences
|July 28, 2026
Summary
Self-injurious behavior (SIB) involves synaptic changes in brain circuits. Researchers found that dampening reward pathways and potentiating aversion pathways may drive SIB, offering new treatment targets.
Area of Science:
- Neuroscience
- Behavioral Science
Background:
- Self-injurious behavior (SIB) is a serious condition prevalent in adolescents and individuals with neuropsychiatric disorders.
- Disruptions in cellular and circuit mechanisms contribute to SIB vulnerability.
Purpose of the Study:
- To investigate synaptic modifications during SIB using an inducible rat model.
- To explore the role of the endopeduncular nucleus (EP) and nucleus accumbens (NAc) in SIB.
Main Methods:
- Induced SIB in rats by inhibiting the EP with muscimol.
- Assessed AMPA receptor subunit 1 (GluA1) expression and phosphorylation in key brain regions (LHb, VTA, NAc, amygdala, mPFC).
- Modulated NAc activity and the mPFC-NAc pathway to observe effects on SIB.
Main Results:
- EP inhibition altered GluA1 expression in the mPFC, VTA, NAc, and amygdala.
- NAc hyperactivation increased SIB at lower EP inhibition levels but not at higher levels.
- Inhibition of the mPFC-NAc pathway exacerbated SIB-related wounds.
- SIB onset correlated with dampened excitatory transmission in reward circuits and potentiation in aversion circuits.
Conclusions:
- SIB is associated with a shift in brain processing from reward to threat.
- Findings suggest novel mechanistic insights into SIB.
- These results may inform future therapeutic strategies for SIB.
