@article{ref1,
title="Serotonergic contributions to human brain aggression networks",
journal="Frontiers in neuroscience",
year="2019",
author="Klasen, Martin and Wolf, Dhana and Eisner, Patrick D. and Eggermann, Thomas and Zerres, Klaus and Zepf, Florian D. and Weber, Rene and Mathiak, Klaus",
volume="13",
number="",
pages="e42-e42",
abstract="Aggressive behavior is associated with dysfunctional frontolimbic emotion regulation circuits. Recent findings suggest serotonin as a primary transmitter for prefrontal amygdala control. However, the association between serotonin levels, amygdala regulation, and aggression is still a matter of debate. Neurobehavioral models furthermore suggest a possible mediating influence of the monoamine oxidase A gene (<i>MAOA</i>) on this brain-behavior relationship, with carriers of low expressing allele varieties being a risk group for aggression. In the present study, we investigated the influence of brain serotonin modulation and <i>MAOA</i> genotype on functional amygdala connectivity during aggressive behavior. Modulation of serotonergic neurotransmission with acute tryptophan depletion (ATD) and placebo were administered in a double-blind, cross-over design in 38 healthy male participants. Aggressive behavior was modeled in a violent video game during simultaneous assessment of brain activation with functional magnetic resonance imaging (fMRI). Trait aggression was measured with the Buss-Perry Aggression Questionnaire (BP-AQ), and <i>MAOA</i> genotypes were assessed from blood samples. Voxel-wise functional connectivity with anatomically defined amygdala was calculated from the functional data. Tryptophan depletion with ATD reduced aggression-specific amygdala connectivity with bilateral supramarginal gyrus. Moreover, ATD impact was associated with trait aggression and <i>MAOA</i> genotype in prefrontal cortex regions. In summary, serotonergic corticolimbic projections contribute to aggressive behavior. Genotype-specific vulnerability of frontolimbic projections may underlie the elevated risk in low expressing allele carriers.<p /> <p>Language: en</p>",
language="en",
issn="1662-4548",
doi="10.3389/fnins.2019.00042",
url="http://dx.doi.org/10.3389/fnins.2019.00042"
}