
Aggression is a complex behavior that involves multiple brain circuits and neurotransmitters, including dopamine. This study highlights how dopamine, through the ventral tegmental area and the dorsal lateral septum, modulates aggression differently depending on the individual's experience.
Aggression is a behavior present in several species, including humans, and can be triggered in situations such as territorial defense, competition for resources or protection of offspring.
Despite being a natural response in certain contexts, its regulation is crucial to avoid excessive or harmful behaviors.
In the brain, several regions participate in the control of aggression, such as the amygdala, which processes emotions; the hypothalamus, involved in automatic defense responses; and the dorsal lateral septum (dLS), known to directly regulate aggressive behaviors.
In addition, the ventral tegmental area (VTA), which controls dopamine release, also plays an important role in modulating aggression, as shown in recent studies.

Dopamine is a neurotransmitter widely known for its role in the reward and motivation system, but it also plays a significant role in regulating social behaviors such as aggression.
Studies indicate that dopaminergic circuits, especially those involving the ventral tegmental area, can either increase or decrease aggression, depending on factors such as the individual's previous experience with aggressive behavior.
This latest research, conducted by researchers at New York University Grossman School of Medicine, USA, investigated how dopamine in the ventral tegmental area regulates aggression in male mice, revealing intriguing mechanisms.
In mice with no previous experience in aggressive behavior, called novice aggressors, dopaminergic cells in the ventral tegmental area play a key role in the initiation and amplification of aggression.
When dopamine synthesis in this region was eliminated, these mice did not develop aggressive behavior, showing that dopamine is essential in the early stage of aggressive behavior.
However, in mice that were already experienced in aggression, known as expert aggressors, dopamine was no longer needed to sustain these behaviors. This suggests that, over time, the brain adapts, and other circuits take over control of aggression, making it independent of dopaminergic modulation in the VTA.

Image: Marisela Morales and M. Flavia Barbano. Neurocircuitry of Addiction 2023, Pages 45-72
The study also revealed that dopamine regulates aggression through the dorsal lateral septum (dLS), a region already known to control these behaviors.
The team also measured dopamine release in the lateral septum as the mice gained fighting experience. They found that the chemical spiked the most on the day they decided to attack for the first time.
As the mice became more experienced in fighting, this dopamine spike became less dramatic, supporting a central role for the chemical in early aggression learning.
Importantly, the researchers also found that dopamine did not appear to play a similar role in female aggression. In fact, manipulating dopamine levels did not affect aggressive behaviors in female mice at all.

In novice aggressors, dopamine allows information from the hippocampus to reach the dLS, reducing local inhibition and facilitating aggressive behavior.
In expert aggressors, this inhibition is already naturally reduced, and the influence of dopamine on the modulation of the dLS decreases significantly. This shows how the role of dopamine in the control of aggression changes with learning and experience.
These results highlight that dopamine not only plays a crucial initial role in the development of aggression, but also that the brain adapts over time, altering the circuits that regulate these behaviors.
This finding is relevant for understanding how aggression works in the human brain, especially in cases of excessive or uncontrolled aggression associated with psychiatric disorders.

Furthermore, the findings open up new possibilities for the development of treatments. Drugs that modulate dopaminergic circuits or the dorsal lateral septum may become effective tools for treating dysfunctional aggressive behaviors.
Another important contribution of this study is the understanding of how the brain adjusts to learned behavior, which may be useful for exploring not only aggression, but also other social behaviors that involve adaptation and experience.
Overall, the study reveals that dopamine plays a sophisticated role in modulating aggression in adult male mice.
While dopamine in the VTA is essential for inexperienced aggressors, it becomes dispensable in experienced aggressors, due to the reconfiguration of brain circuits.
These results offer new insights into the neural mechanisms of aggression and provide a basis for exploring therapeutic strategies in humans.
READ MORE:
Experience-dependent dopamine modulation of male aggression.
Bing Dai, Bingqin Zheng, Xiuzhi Dai, Xiaoyang Cui, Luping Yin, Jing Cai, Yizhou Zhuo, Nicolas X. Tritsch, Larry S. Zweifel, Yulong Li & Dayu Lin
Nature (2025).
Abstract:
Numerous studies support the role of dopamine in modulating aggression1,2, but the exact neural mechanisms remain elusive. Here we show that dopaminergic cells in the ventral tegmental area (VTA) can bidirectionally modulate aggression in male mice in an experience-dependent manner. Although VTA dopaminergic cells strongly influence aggression in novice aggressors, they become ineffective in expert aggressors. Furthermore, eliminating dopamine synthesis in the VTA prevents the emergence of aggression in naive mice but leaves aggression intact in expert aggressors. VTA dopamine modulates aggression through the dorsal lateral septum (dLS), a region known for aggression control. Dopamine enables the flow of information from the hippocampus to the dLS by weakening local inhibition in novice aggressors. In expert aggressors, dLS local inhibition naturally weakens, and the ability of dopamine to modulate dLS cells diminishes. Overall, these results reveal a sophisticated role of dopamine in the rise of aggression in adult male mice.
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