Role of serotonin and dopamine system interactions in the neurobiology of impulsive aggression and its comorbidity with other clinical disorders

Seo, Dongju; Patrick, Christopher J.; Kennealy, Patrick J.

doi:10.1016/j.avb.2008.06.003

Cited by 520Neurotransmitter Receptor Influence on BehaviorNeural and Behavioral Psychology StudiesPsychopathy, Forensic Psychiatry, Sexual Offending

Role of serotonin and dopamine system interactions in the neurobiology of impulsive aggression and its comorbidity with other clinical disorders

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Seo, Dongju, Patrick, Christopher J., Kennealy, Patrick J.·2008·Aggression and Violent Behavior

DOI 10.1016/j.avb.2008.06.003PMC PMC2612120

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Abstract

Impulsive aggression is characterized by an inability to regulate affect as well as aggressive impulses, and is highly comorbid with other mental disorders including depression, suicidal behavior, and substance abuse. In an effort to elucidate the neurobiological underpinnings of impulsive aggression and to help account for its connections with these other disorders, this paper reviews relevant biochemical, brain imaging, and genetic studies. The review suggests that dysfunctional interactions between serotonin and dopamine systems in the prefrontal cortex may be an important mechanism underlying the link between impulsive aggression and its comorbid disorders. Specifically, serotonin hypofunction may represent a biochemical trait that predisposes individuals to impulsive aggression, with dopamine hyperfunction contributing in an additive fashion to the serotonergic deficit. The current paper proposes a modified diathesis-stress model of impulsive aggression in which the underlying biological diathesis may be deficient serotonergic function in the ventral prefrontal cortex. This underlying disposition can be manifested behaviorally as impulsive aggression towards oneself and others, and as depression under precipitating life stressors. Substance abuse associated with impulsive aggression is understood in the context of dopamine dysregulation resulting from serotonergic deficiency. Also discussed are future research directions in the neurobiology of impulsive aggression and its comorbid disorders.

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Alcohol can further suppress prefrontal inhibitory processes while potentiating limbic activation, creating a vicious cycle wherein aggression and heavy drinking reinforce one another.
“Alcohol can further suppress prefrontal inhibitory processes while potentiating limbic activation, creating a vicious cycle wherein aggression and heavy drinking reinforce one another (Seo et al. 2008; Heinz et al. 2011).”
From Decoding the bidirectional links between alcohol misuse and aggression: toward a unified translational framework (2026) · cites this paper as Seo et al. 2008
In “Substance Abuse and Impulsive Aggression” (page unavailable), the paper links prefrontal dysfunction, elevated limbic dopamine activity, and poor inhibition with substance abuse and impulsive aggression, particularly in type II alcoholism. It does not establish that alcohol itself further suppresses prefrontal inhibition or potentiates limbic activation, or that aggression and heavy drinking form a reciprocal reinforcing cycle. (LLM, conf=0.84)
Experimental — accuracy not yet measured
These circuits are modulated by serotonergic and dopaminergic dysfunction: serotonin deficits are associated with impulsive aggression, while dopamine dysregulation drives increased reward sensitivity and dysregulated motivational drive toward substance use.
“These circuits are further modulated by serotonergic and dopaminergic dysfunction: serotonin deficits are associated with impulsive aggression, while dopamine dysregulation drives increased reward sensitivity and dysregulated motivational drive toward substance use (Seo et al. 2008; Gan et al. 2015b).”
From Decoding the bidirectional links between alcohol misuse and aggression: toward a unified translational framework (2026) · cites this paper as Seo et al. 2008
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Dopamine neuronal cell bodies and axon terminals are modulated by 5-HT and receive extensive projections from these neurons.
“As evident in past studies, DA neuronal cell bodies and axon terminals are modulated by 5-HT and receive extensive projections from these neurons (54).”
From Emotional Blunting in Patients With Major Depressive Disorder: A Brief Non-systematic Review of Current Research (2021) · cites this paper as [54]

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Authors: Seo, D., Patrick, C. J., & Kennealy, P. J.
Affiliations: University of Minnesota (US)
University of California, Irvine (US)
Corresponding author: Seo, Dongju
ORCID: Seo, Dongju
Patrick, Christopher J.
Kennealy, Patrick J.
Venue: Aggression and Violent Behavior
Publisher: Elsevier BV
Published: 2008-10
Volume: 13
Issue: 5
Pages: 383-395
ISSN: 1359-1789 (ISSN-L)
DOI: 10.1016/j.avb.2008.06.003
PMC: PMC2612120
OpenAlex: W2087778925
Semantic Scholar: 917e33714300de26daabf9c7aac98620f86c211a
Cited by: 520
References: 168
Citations by year: 2026: 26 · 2025: 44 · 2024: 30 · 2023: 40 · 2022: 34 · 2021: 36 · 2020: 35 · 2019: 26 · 2018: 41 · 2017: 33 · 2016: 30 · 2015: 34 · 2014: 27 · 2013: 23 · 2012: 21
FWCI: 5.77
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Aggression and Violent Behavior (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of Mental Health (P50MH072850, R21MH065137)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
Social Sciences › Psychology › Clinical Psychology › Psychopathy, Forensic Psychiatry, Sexual Offending
Keywords: impulsive aggression, serotonin, dopamine, serotonin-dopamine interaction, prefrontal cortex, ventral prefrontal cortex, diathesis-stress model, depression, suicidal behavior, substance abuse, comorbidities, neurobiology of aggression

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Role of serotonin and dopamine system interactions in the neurobiology of impulsive aggression and its comorbidity with other clinical disorders

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