Mesocorticolimbic dopamine functioning in primary psychopathy: A source of within-group heterogeneity

• Primary psychopathy can be situated on a continuum spanning from controlled to disinhibited.
• Serotonergic hyperstability mediates the emotional deficiency in primary psychopathy.
• Primary psychopathy is generally related to higher tonic/population activity of mesolimbic DA.
• However, pathologically heightened mesolimbic DA increases the risk for disinhibited subtypes.
• In addition, mesocortical DA hypofunctionality further increases risk for disinhibited subtypes.

Despite similar emotional deficiencies, primary psychopathic individuals can be situated on a continuum that spans from controlled to disinhibited. The constructs on which primary psychopaths are found to diverge, such as self-control, cognitive flexibility, and executive functioning, are crucially regulated by dopamine (DA). As such, the goal of this review is to examine which specific alterations in the meso-cortico-limbic DA system and corresponding genes (e.g., TH, DAT, COMT, DRD2, DRD4) might bias development towards a more controlled or disinhibited expression of primary psychopathy. Based on empirical data, it is argued that primary psychopathy is generally related to a higher tonic and population activity of striatal DA neurons and lower levels of D2-type DA receptors in meso-cortico-limbic projections, which may boost motivational drive towards incentive-laden goals, dampen punishment sensitivity, and increase future reward-expectancy. However, increasingly higher levels of DA activity in the striatum (moderate versus pathological elevations), lower levels of DA functionality in the prefrontal cortex, and higher D1-to-D2-type receptor ratios in meso-cortico-limbic projections may lead to increasingly disinhibited and impetuous phenotypes of primary psychopathy. Finally, in order to provide a more coherent view on etiological mechanisms, we discuss interactions between DA and serotonin that are relevant for primary psychopathy.