Which neurotransmitters are involved in hostility

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Does free will exist? Do humans have the ability to choose between what we consider good and evil, between moral and immoral behavior? The great majority of people in the world believe this to be the case. But until not very long ago we believed that infections were a divine punishment and that epilepsy was a sign of demonic possession. Are we on the cusp of viewing criminal or just plain nasty behavior as being biologically determined?

We have lesioning or DBS for movement disorders, well-established. Brain surgery for pain? Psychiatric surgery? But surgery for aggression? This is the third rail of stereotactic and functional neurosurgery. Read this paper, and open your minds. Consider the patients who are referred for this surgery. More recently, imaging studies have identified the neural circuits that become activated in the brains of normal, healthy individuals during moral decision-making.

The analysis was undertaken to see if the brain regions compromised in antisocial populations include the newly identified brain regions involved in moral decision-making. Raine and his colleagues compared the brain images of antisocial individuals with control subjects. They found that antisocial individuals also tended to have overlapping damage in brain structures involved in making moral judgments, most notably the dorsal and ventral prefrontal cortex, the amygdala, and the angular gyrus.

New studies from the University of California, San Diego, are helping scientists better understand what goes on in the brains of some teenage boys who respond with inappropriate anger and aggression to perceived threats. Preliminary findings from these studies suggest that such behavior is associated with a hyperactive response in the amygdala, an area of the brain that processes information regarding threats and fear, and with a lessening of activity in the frontal lobe, a brain region linked to decision-making and impulse control.

Aggressive behavior can be divided into two types: proactive and reactive. Proactive aggressors plan how they're going to hurt and bully others. Reactive aggression, however, is not premeditated; it occurs in response to an upsetting trigger from the environment. Their behavior is emotionally 'hot,' defensive, and impulsive. The term "reactive-affective-defensive-impulsive" RADI has recently been created to describe such behavior. Research suggests that adolescents with RADI behavior are at an increased risk for a lifetime of problems associated with impulsive aggression.

Little is known about how the brain works in reactive aggression. In their most recent studies, Frank and his colleagues recruited two groups of male adolescents: one group diagnosed with RADI behavior and the other group without any history of mental illness or aggression problems.

While being scanned by a brain imaging machine, both sets of teenagers were asked to perform tasks that involved reacting to age-appropriate, fear-inducing images. The tasks also tested the teenagers' impulsivity. Preliminary data reveal that the brains of RADI teenagers exhibited greater activity in the amygdala and lesser activity in the frontal lobe in response to the images than the brains of the teenagers in the control group.

In a related study, Frank and his colleagues are investigating whether these changes in brain activity are associated with an abnormal increase in cortisol levels, a marker of the stress response. The brain chemical serotonin has long been known to play an important role in regulating anger and aggression. Low cerebrospinal fluid concentrations of serotonin have even been cited as both a marker and predictor of aggressive behavior.

New studies from the Netherlands, however, indicate that this serotonin-deficiency hypothesis of aggressiveness may be too simple. Furthermore, research now suggests that unchecked aggressive behavior can eventually change the brain in ways that cause serotonin activity to decrease-and, perhaps, violent behavior to increase. To perform their most recent studies, de Boer and his colleagues engendered violent characteristics of aggressive behavior in feral mice and rats by permitting them to physically dominate other rodents repeatedly.

With such positive reinforcement, the animals' initially normal aggressiveness gradually became transformed into a more pathological form-the kind also seen in pathologically violent people. During this transformation, de Boer studied the chemical changes that occurred in the rodents' aggression-related brain circuits, particularly those circuits involved with serotonin. They found that serotonin activity decreased as a result of the animals experiencing repeated victorious episodes of aggression but not as a result of normal, functional acts of aggression.

More recently, de Boer and his colleagues have found that the transition from normal, adaptive aggressive behavior into abnormal forms that inflict harm and injury is due to functional, but not structural, changes in certain serotonin receptors in the brain. In animal studies, treatment with selective serotonin receptor agonist compounds has been found to restore the normal function of these receptors-and suppress aggressive behavior, including its escalated forms.

These findings may one day lead to more effective treatments for violent behavior in humans. How do some of us manage to control our violent tendencies while others cannot? She and her team of international collaborators found that an increase in the levels of two neurotransmitters, glutamate and serotonin, in key parts of the brain is linked to intense aggression in male mice.

In mice, especially in males, as in many other animal species, aggressive behaviors have evolved as adaptations to deal with danger and with competition for resources such as mates, food and shelter. When this adaptive species-typical aggression escalates to intense aggression, it becomes destructive or maladaptive. Due to similarities in the neurobiology of aggression between rodents and humans, studies in mice may eventually help us to understand and even treat antisocial, violent and psychopathic behavior in humans.

Dr Takahashi's research, recently published in the Journal of Neuroscience , focused on a part of the brain called the dorsal raphe nucleus DRN. The DRN is located in the lower, most primitive part of the brain and contains the largest collection of serotonin-producing neurons in the brain.

Serotonin, sometimes known as the 'happiness hormone', has been implicated in the control of aggression more than any other molecule in the brain, in several species ranging from invertebrates to humans.

The DRN receives glutamate from many brain areas, including the medial pre-frontal cortex, a part of the brain targeted in the procedure known as frontal lobotomy. Several types of psychiatric illnesses such as anxiety disorders and depression, as well as aggression, are linked to an imbalance between the levels of glutamate and GABA. Measuring aggression in mice involves introducing an intruder mouse into a resident mouse's homecage and observing the type and levels of aggression that ensue.

For example, normal aggressive behavior includes threatening postures and acts while escalated aggression results in an increased frequency and intensity of biting. For the first time, an in vivo microdialysis study, in which the DRN areas of the brains of living mice were implanted with a probe that can both microinject drugs and collect samples of brain fluid, showed changes in glutamate input in the DRN during aggressive behavior in male mice.

Using a clever combination of genetically-engineered mice and in vivo microdialysis, the researchers showed that glutamate release increased in the DRN during an aggressive encounter. Serotonin release was also increased within the DRN, as well as in the medial pre-frontal cortex during escalated aggression, but this increase in serotonin release was not observed when animals were engaged in normal adaptive aggression.

Glutamate input to the DRN is thus critical for an escalation in aggressive behavior, and causes a surge in serotonin. The precise role of this glutamate input, as well as its origin, remains to be clarified. Studies such as this may provide in future the targets needed to develop therapeutic interventions for those of us with extreme antisocial behaviors and psychiatric illnesses. Takahashi, Assistant Professor in the Laboratory of Behavioral Neuroendocrinology, fell in love with the Japanese Fancy Mouse, a mouse strain used in this type of research, when she was a graduate student in the University of Tsukuba and visited Dr.

Koide at his laboratory. This mouse was domesticated as a pet in Japan a few hundred years ago. She then decided to change her major from psychology to behavioral genetics. She said "I'm interested in the mechanism of escalating an adaptive species-typical aggressive behavior.

From this research we plan to examine which activation pattern or inhibition of the serotonin system can affect which type of aggression.