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For all animals, varying moods and emotions appear to be very complex behaviors controlled by many different parts of the human brain. Researchers have known that these aspects of behavior are controlled by neurotransmitters, such as serotonin and norepinephrine, in the brain. These transmitters can be broken down by the enzyme, monoamine oxidase A (MAO-A). In a new study, researchers looked at the enzyme that regulates MAO-A with the hopes of creating potential new treatments for mental disorders.

In this new study, the research team composed of Jun Aruga and colleagues from the RIKEN Brain Science Institute focused on the pathway that regulates the metabolism of MAO-A. This pathway, known as the ubiquitin-proteasome pathway, is in charge of moving old, misfolded or any other unwanted molecules to what is understood as the cellular trash can. The researchers started their study by reproducing mice that did not have the gene responsible for encoding the enzyme, Rines E3 ubiquitin ligase. This enzyme helps pick out which proteins will be destroyed.

The researchers found that mice that did not have the enzyme had a very drastic change in their emotional behavior. These mice were a lot more reluctant in exploring other new environments. They also were also less likely to spend time in open spaces in comparison to healthy mice. These behavioral changes indicate that the mice suffered from more anxiety and had an abnormal stress response.

The researchers proceeded to observe the brain chemistry of these mice. They found that these genetically altered mice had reduced levels of serotonin and norepinephrine in the sections of the brain that are responsible for regulating emotion and stress response. These regions include the locus ceruleus, prefrontal cortex and amygdala.

"The next step is to clarify the change in emotional response abnormalities using the animals' personal history," stated Aruga.  "Studies in humans indicate that the prevalence of aggressive and antisocial behavior in adults with the low-level MAO-A variant is affected by their history of stress during childhood, so personal history and gene-environment interaction studies with the mutant mice would contribute to a more comprehensive understanding of the pathophysiology of aggression and antisocial behavior."

This study was published in the Journal of Neuroscience.