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A recent [(18)F]FDOPA-PET study reports negative correlations between dopamine synthesis rates and aggressive behavior. Since dopamine is among the substrates for monoamine oxidase A (MAOA), this investigation examines whether functional allelic variants of the MAOA tandem repeat (VNTR) promotor polymorphism, which is known to modulate aggressive behavior, influences dopamine release and aggression in response to violent visual stimuli. We selected from a genetic prescreening sample, strictly case-matched groups of 2×12 healthy male subjects with VNTRs predictive of high (MAOA-High) and low (MAOA-Low) MAOA expression. Subjects underwent pairs of PET sessions (dopamine D2/3 ligand [(18)F]DMFP) while viewing a movie of neutral content, versus violent content. Directly afterwards, aggressive behavior was assessed by the Point Subtraction Aggression Paradigm (PSAP). Finally, PET data of 23 participants and behavioral data of 22 participants were analyzed due to post hoc exclusion criteria. In the genetic prescreening sample MAOA-Low carriers had significantly increased scores on the Buss-Perry Aggression Questionnaire. In the PET-study-group, aggressive behavior under the emotional neutral condition was significantly higher in the MAOA-Low group. Interestingly, the two MAOA-groups showed inverse dopaminergic and behavioral reactions to the violent movie: The MAOA-High group showed higher dopamine release and increased aggression after the violent movie; MAOA-Low subjects showed decreases in aggressive behavior and no consistent dopamine release. These results indicate a possible impact of the MAOA-promotor polymorphism on the neurobiological modulation of aggressive behavior. However, the data do not support approaches stating that MAOA-Low fosters aggression by a simple pro-dopaminergic mechanism., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Imaging of cerebral A(1) adenosine receptors (A(1)AR) with positron emission tomography (PET) has recently become available for neurological research. To date, it has still not been unraveled if there is a valid reference region without specific radioligand binding that may be used to improve image quantification. We conducted in vivo displacement studies in humans to elucidate this important question using the A(1)AR ligand [(18)F]CPFPX., Methods: Five healthy male volunteers underwent [(18)F]CPFPX bolus/infusion PET with short infusion of unlabelled CPFPX as competitor (n = 4; 0.9 to 4.0 mg) or vehicle (n = 1; control condition) after equilibrium of [(18)F]CPFPX distribution was attained., Results: Infusion of CPFPX induced a rapid displacement of [(18)F]CPFPX binding in all regions, including the cerebellum (region with lowest binding). Even at the highest competitor dose, no full displacement was reached. Displacement was dose-dependent in all regions except the cerebellum where floor effects and/or noise might have obscured dose dependency. Specific binding was estimated to account for about one third and two thirds of total equilibrium uptake in cerebellum and cortex, respectively., Conclusions: Although the cerebellum is the region with lowest in vivo [(18)F]CPFPX binding, it is not an ideal reference region devoid of specific binding. Nevertheless, as will be discussed, the use of a reference region analysis may be a useful, non-invasive alternative analysis method in carefully selected applications.