Extremely interesting and important results were demonstrated by experiments on the use of anti-aggressive agents in mice and rats. It turned out that some of them are capable of reducing the manifestation of attacking aggression on their part, while not affecting defensive aggression and other non-aggressive forms of behavior and social communication. To be more specific, we are talking about agonists that activate serotonin 5-HT1A/1B receptors.
These results align with the theory that many species possess innate inhibitors of aggressive behavior, which prevent causing harm and killing members of their own species. In the case of humans, a model of the violence inhibition mechanism (VIM) was even developed, which also explains the development of empathy. Based on this theory, violence in intraspecific relationships should be viewed as a pathological rather than a natural form of behavior. Especially since even in many territorial, social, and armed species, the level of lethal violence still does not exceed 1%, and according to various evidence, only no more than 2% of people do not experience strong resistance to committing murder.
We also see that defensive aggression, unlike attacking aggression, is indeed a natural form of behavior, and the work of the violence inhibitor does not stop it in the presence of an immediate threat to life in the environment. This was well demonstrated by the administration of the 5-HT1A agonist alnespirone to rats. It had an extremely selective effect; the strong reduction in aggressiveness did not prevent the rats from resorting to defensive behavior when encountering an aggressive peer.
Various genetic evidence demonstrates that certain variants of the 5-HT1A/1B receptor genes, as well as three other genes associated with the 5-HT system—TPH2, MAO A (also known as the “warrior gene”), and SERT—lead to increased aggressiveness in animals and humans. For example, in one study, impulsive and aggressive alcoholics were found to have differences in the 5-HT1B gene compared to healthy people and non-aggressive alcoholics. This study covered two different groups of people: Finns and a Native American tribe. Mutations in the MAO A gene have long been known as a cause of abnormal manifestations of aggression in men.
According to the violence inhibition mechanism model, the direct result of its dysfunction is calloused-unemotional (CU) traits in children and psychopathy in adults. Changes in the function of 5-HT1B receptors in certain parts of the brain were found in people with aggressive traits and psychopathic traits. A difference in the 5-HT1B gene genotype was present in children with calloused-unemotional traits.
It should be noted that dozens of genes and a large number of systems influence aggressiveness. However, the violence inhibitor remains a specific mechanism expressed by a limited number of receptors and genes. Firstly, this is simply important for inhibiting aggression most effectively. Secondly, other forms of pharmacological intervention, such as the use of antipsychotics (like haloperidol), beta-blockers, drugs affecting GABA neurotransmitters, and 5-HT2 receptor agonists and antagonists (many psychedelics belong to the former), result only in a non-selective reduction of aggressiveness, suppressing defensive aggression and other forms of behavior, and causing side effects.
Understanding the nature of the violence inhibitor and its limitation to a small number of receptors and genes can not only tell us a lot about violence itself, but also help in creating a solution aimed against it as a pathological form of behavior inherent in a minority of people. And the essence of such a solution is simple: returning to them the inhibiting control over aggression that is natural for the majority, through the use of appropriate pharmacological or even gene-therapeutic drugs.
This material briefly describes the content of the article titled “Neurophysiology and Genetics of the Violence Inhibition Mechanism“, which you may refer to for greater detail.
