The recent discovery of neurons with mirroring properties in the mouse ventromedial hypothalamus (VMHvl) offers a new perspective on the origin and function of mirror neurons, traditionally associated with empathic and complex behaviors in primate neocortical regions. Contrary to previous concepts that positioned mirror neurons as byproducts of associative learning in more recent brain areas, the data presented by Yang et al. suggest that such mechanisms already existed in phylogenetically ancient brain structures, with central survival functions such as territorial aggression.
Using fiber photometry and miniscope imaging techniques, the authors demonstrated that certain VMHvl neurons activate both when the animal engages in aggressive behavior and when it simply observes a fight between third parties. This response was not attributed to behavioral mimicry or pheromone activation, as would be expected in rodents, since even mice genetically engineered to be anosmic (Trpc2–/–) showed neuron activation when observing aggression from others. This indicates that activation is predominantly visual and does not depend on prior experience or associative learning with aggressive behavior (Ferrari et al., 2023).
This finding is significant not only because it expands the anatomical location of mirror neurons to the hypothalamus—a structure associated with instinctual behaviors such as feeding, sleeping, and reproduction—but also because it implicates these neurons in innate, stereotyped responses. Furthermore, chemogenetic manipulation of these cells has shown that their inhibition reduces aggression, while their activation intensifies it, even directing aggressive behavior toward one’s own reflection in the mirror. This suggests that these neurons are both necessary and sufficient for the expression of aggression, configuring a neural circuit deeply rooted in the biology of survival (Ferrari et al., 2023).
The hypothesis that mirror neurons in the neocortex arose as an epigenetic consequence of development—rather than a direct product of natural selection—is challenged by the data presented. The presence of mirroring mechanisms in hypothalamic centers conserved throughout evolution points to a more comprehensive model, in which different types of mirror neurons evolved in a mosaic manner, with multiple origins and contextually modulated functions. While more recent neocortical systems exhibit plasticity and dependence on individual experience, hypothalamic systems operate rigidly, activating stereotyped behavioral patterns in response to key stimuli—similar to the “signal stimuli” defined in classical ethology (Ferrari et al., 2023).
Equally important is the impact of this discovery on the interpretation of the role of mirror neurons in empathy. Traditionally seen as mediators of emotional understanding and imitation, mirror neurons are now also shown to be involved in the activation of socially disruptive behaviors, such as aggression. This suggests that the neural mechanisms underlying empathy and violence may share common neural circuits, whose activation depends on specific environmental contexts and adaptive pressures. This ambivalence—or, as the article puts it, the “dark side” of mirror neurons—requires a rethinking of simplistic conceptions that automatically associate these cells with empathic processes (Ferrari et al., 2023).
By revealing the presence of mirror neurons in the VMHvl with a key role in aggression, this study not only illuminates fundamental aspects of the neurobiology of social behavior but also provides a solid foundation for understanding how primitive and robust neural circuits shape behavioral responses critical to survival and social organization. Personally, reading this article, I noted how the dichotomy between empathy and aggression, often viewed as antagonistic, may be rooted in shared neural mechanisms, dependent on contextual and phylogenetic factors.
Reference:
FERRARI, Pier Francesco; MÉNDEZ, Carlos Andrés; COUDÉ, Gino. Aggression: The dark side of mirror neurons sheds light on their functions. Current Biology, v. 33, n. 8, p. R296–R318, 2023. DOI: https://doi.org/10.1016/j.cub.2023.03.028.
