Animal models have allowed researchers to study the role of genes and neurochemistry in human aggression. One of the ways that this happens is when a behaviour is observed in humans and a polymorphism (genetic mutation) is noted when the individual's genome is sequenced.  Researchers then attempt to replicate that mutation in an animal model to see if the results are the same. 

Modern research often uses transgenic mice – that is, mice that have been artificially modified at a genetic level to include a foreign sequence, or transgene. This often involves the insertion of a human gene into the mouse’s genome to create a humanized mouse. One method of creating transgenic mice involves the delivery of the transgene into a single cell of the mouse embryo.

An example of how transgenic mice have been used to study the potential link between a human genetic mutation and aggressive behaviour started with research done by Brunner (1993).  Brunner studied a Dutch family in which 28 of the male family members were repeatedly involved in impulsively aggressive violent criminal behaviour. When assessed by clinical psychiatrists, there was no specific psychiatric diagnosis.

Brunner and his team were able to sample genetic material from the family.  The researchers found a variation in the gene that produces monoamine oxidase A (MAOA), an enzyme that affects the neurotransmitters dopamine, norepinephrine, and serotonin. The variation results in low levels of the MAOA enzyme and raised levels of serotonin, dopamine, and norepinephrine. Brunner (1996) argued, however, that because genes are essentially simple and behaviour is by definition complex, a direct causal relationship between a single gene and a specific behaviour is highly unlikely.

Through the media, the gene quickly became known as "the warrior gene." A study done by McDermott et al (2009) wanted to see if the gene actually had an impact on behaviour. To do so, they carried out an experiment with people with both a "normal" genotype and a variation of the MAOA gene. In this experiment, participants punished opponents that they believed had cheated them out of money by giving them different amounts of very spicy hot sauce.  They found that those with the variation were more likely to give the opponent a higher amount of the hot sauce. 

A more recent study by Tiihonen et al (2014) found a link between two specific genes and a person’s likelihood to commit a violent crime. The researchers examined patterns of criminal behavior and genetics in the Finnish population and found that a variation of the MAOA gene was present in the genomes of up to 10% of all violent offenders. However, people who committed non-violent crimes did not have a higher-than-normal prevalence of these genes.

But is this type of research enough?  It is all part of the bigger study of the "warrior gene." A study by Cases et al (1995) was able to test the variation in mice.  This is important support for the theory of a genetic root of aggression in humans.

Cases et al (1995) carried out a study on the genetic origins of aggression. For their study, they used a transgenic mouse where the gene that regulates the production of monoamine oxidase A (MAOA), an enzyme that breaks down serotonin and norepinephrine, was ‘knocked out” or deleted.

Between days 11 and 16, the transgenic mice showed several signs of low MAOA, including frantic running, violent shaking during sleep and a tendency to bite the experimenter. In adult males, they observed signs of offensive aggressive behaviour - including bite wounds.

To test the effect of the genetic variation, the researchers carried out "resident-intruder" tests, where a mouse was introduced into the cage of another mouse. With control mice, when the "intruder" was introduced, the mice would "check out" the other mouse, sniffing and engaging with the mouse.  In the transgenic mice, the mice adopted a threatening hunched position and would engage in aggressive behaviour.  This was also true in the case where the intruder was a female mouse.

Autopsies of the brains of the mice showed an increase in serotonin, dopamine, and norepinephrine.  Although dopamine was not highly elevated, serotonin levels were six to nine times higher than the control mice.

The study showed that the genetic variation led to MAOA deficient mice that exhibited strong aggressive behaviour.  The researchers concluded that when human males lack MAOA and demonstrate aggressive behaviour, the behaviour cannot be attributed to social factors. Instead, the MAOA deficiency is a predisposition toward aggressive behaviour which may be expressed through interaction with social and environmental factors.

Research such as Caspi et al (2002), McDermott et al (2009) and Tiihonen et al (2014) all appear to confirm the animal model.  It appears that the findings in animal research reflect what we see in human behaviour.

Although the research confirms human research, it is still questionable whether an animal model truly reflects the types of aggression that we see in humans.

It is believed that the majority of people who have the MAOA polymorphism do not exhibit aggressive behaviour.  This does not mean that the gene does not have this potential effect on human behaviour, but it means that there must be a gene x environment interaction for the behaviour to occur.

The study is experimental, so a cause and effect relationship can be established.  This type of cause and effect relationship could not be studied in human participants.

There are ethical concerns about using animals in such a manner, leading to permanent damage.

Tiihonen, J., Rautiainen, M., Ollila, H. M., Repo-Tiihonen, E., Virkkunen, M., Palotie, A., . . . Paunio, T. (2014). Genetic background of extreme violent behavior. Molecular Psychiatry, 20(6), 786-792. doi:10.1038/mp.2014.130