Neural reactivity to rewards and losses in offspring of mothers and fathers with histories of depressive and anxiety disorders.

Children of parents with depression exhibit neural abnormalities in reward processing. Examining contributions of parenting could provide insight into the development of these abnormalities and to the etiology of depression. We evaluated whether early parenting moderates the effects of parental depression on a neural measure of reward and loss processing in mid-late childhood. Parenting was assessed when children were preschoolers. At age nine, children completed an event-related potential assessment and the feedback negativity (FN) was measured following rewards and losses (N=344). Maternal authoritative parenting moderated the effect of maternal depression; among offspring of mothers with histories of depression, low authoritative parenting predicted a blunted FN. Observed maternal positive parenting interacted with paternal depression in a comparable manner, indicating that maternal parenting may buffer the effects of paternal depression. Early parenting may be important in shaping the neural systems involved in reward processing among children at high risk for depression.

Objective: Reward-processing abnormalities are thought to be a key feature of various psychiatric disorders and may also play a role in disruptive mood dysregulation disorder (DMDD), a new diagnosis in DSM-5. In the current study, we used eventrelated potentials (ERP) sensitive to monetary gains (i.e., the reward positivity [RewP]) and losses (i.e., the N200) to examine associations between symptoms of DMDD during early childhood and later reward processing during preadolescence. Methods: To assess early emerging DMDD symptoms in a large longitudinal community sample (n = 373) of 3-year old children, we administered a diagnostic interview, Preschool Age Psychiatric Assessment (PAPA) with parents. At a later assessment, *6 years later, children completed a monetary reward task while an electroencephalogram (EEG) was recorded. Children's lifetime history of psychopathology was also assessed at that time using Kiddie-Schedule of Affective Disorders and Schizophrenia (K-SADS) with the child and parent. Results: Multiple regression analyses revealed that age 3 DMDD symptoms predicted an enhanced RewP to monetary rewards in preadolescence. This association is independent of demographics and lifetime history of symptoms of depression, any anxiety disorder, attention-deficit disorder, oppositional defiant disorder, or conduct disorder Conclusions: Early manifestations of DMDD in children as young as 3 years old predicted enhanced reward processing later in development. These findings add to the growing corpus of literature on the pathophysiology of DMDD, and underscore the predictive validity of preschool DMDD on a neural level.

Motivational and hedonic impairments are core aspects of a variety of types of psychopathology. These impairments cut across diagnostic categories and may be critical to understanding major aspects of the functional impairments accompanying psychopathology. Given the centrality of motivational and hedonic systems to psychopathology, the Research Domain Criteria (RDoC) initiative includes a "positive valence" systems domain that outlines a number of constructs that may be key to understanding the nature and mechanisms of motivational and hedonic impairments in psychopathology. These component constructs include initial responsiveness to reward, reward anticipation or expectancy, incentive or reinforcement learning, effort valuation, and action selection. Here, we review behavioral and neuroimaging studies providing evidence for impairments in these constructs in individuals with psychosis versus in individuals with depressive pathology. There are important differences in the nature of reward-related and hedonic deficits associated with psychosis versus depression that have major implications for our understanding of etiology and treatment development. In particular, the literature strongly suggests the presence of impairments in in-the-moment hedonics or "liking" in individuals with depressive pathology, particularly among those who experience anhedonia. Such deficits may propagate forward and contribute to impairments in other constructs that are dependent on hedonic responses, such as anticipation, learning, effort, and action selection. Such hedonic impairments could reflect alterations in dopamine and/or opioid signaling in the striatum related to depression or specifically to anhedonia in depressed populations. In contrast, the literature points to relatively intact in-the-moment hedonic processing in psychosis, but provides much evidence for impairments in other components involved in translating reward to action selection. Particularly, individuals with schizophrenia exhibit altered reward prediction and associated striatal and prefrontal activation, impaired reward learning, and impaired reward-modulated action selection.