Limitations of the neurophysiological and genetic nature of the violence inhibit

Started by Volunto, Feb 07, 2023, 06:56 PM

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Earlier we mentioned that for effective regulation of aggression, the number of genes and neurotransmitters involved in this process should be limited. Of course, dozens of genes, as well as many systems and receptors, have a certain influence on aggression. However, this is not so important within the framework of the topic we are considering since we are specifically interested in the violence inhibitor as a mechanism that inhibits offensive aggression. To confirm its limited to 5-HT1A and 5-HT1B receptors neurophysiological and genetic nature, one might consider what the attempt to suppress aggressive behavior by pharmacological interaction with other systems influencing aggression leads to.

Dopamine receptor antagonists such as chlorpromazine and haloperidol are widely used in the treatment of aggressive patients. However, these are antipsychotic drugs that suppress nervous activity, which leads to the suppression of defensive aggression and other side effects. Barbiturates and benzodiazepines, which affect the function of GABA receptors, face the same problems, which also severely limits their potential as anti-aggressive agents. Beta-blockers such as propranolol and nadolol are only effective in some patients, such as those with organic brain syndromes and chronic psychosis, and also lead to side effects. Serotonin reuptake inhibitors, which block the function of the serotonin transporter, showed to be effective in reducing aggressiveness in patients with borderline personality disorder. Yet they cannot selectively reduce aggressiveness due to the influence on other forms of behavior and having serious side effects. Finally, agonists and antagonists of 5-HT2 receptors are also able to reduce aggressiveness, however, the former lead to side effects, while the influence of the latter is still very poorly understood. It should be noted that 5-HT2A agonists include many psychedelics known for their anti-aggressive and empathic effects. However, their influence can hardly be called selective.

Based on this, it is 5-HT1A and 5-HT1B agonists that seem to be the most promising drugs in the treatment of aggressiveness since they have an extremely selective effect without affecting defensive aggression and other forms of behavior. This opinion is also shared by some researchers who support the resumption of research on the development of such anti-aggressive agents (or so-called "serenics"). Some of them claim that "modern research suggests that aggressive behavior should be studied as a separate functional disorder" and "it is hoped that new insights into the neurobiology of aggression will reveal novel avenues for treatment of this destructive and costly behavior" (by aggressive behavior they mean the disinhibited one).

It is also very important to note that activation of these receptors has exactly the effect that is expected from the violence inhibitor, while the pharmacological interaction with other systems influencing aggressiveness has a different, non-selective effect. This may confirm the limited neurophysiological and genetic nature of the violence inhibition mechanism, where only a few genes and receptors play a key role.