Acute and Lifetime Stress and Psychotic Illness: The Roles of Reward and Salience Networks

Abstract

Affective reactions to acute stressors often evoke exacerbations of psychotic symptoms and sometimes de novo psychotic symptoms and initial psychotic episodes. Across the lifespan, affective reactions to acute stressors are enhanced by successive adverse childhood experiences (ACEs), in a process called “behavioral sensitization”. The net effects of behavioral sensitization of acute stress responses are to alter responsivity to positive and negative feedback and to unexpected events, regardless of valence, leading to the maladaptive assignment of salience to stimuli and events. The assignment of “aberrant” salience to stimuli and events has profound consequences for learning and decision-making, which can influence both the positive and negative symptoms of psychosis. In this review, we discuss some of the psychological and neural mechanisms by which affective reactivity to acute stress, and its sensitization through the experience of stress and trauma across the lifespan, impact both the positive and negative symptoms of psychosis. We recount how the reward and salience networks of the brain, together with inputs from the dopamine and serotonin neurotransmitter systems, are implicated in both affective reactivity to stress and the symptoms of psychosis, likely mediate the effects of stress and trauma on the symptoms of psychosis and could serve as targets for interventions.

Failure to mate enhances investment in behaviors that may promote mating reward and impairs the ability to cope with stressors via a subpopulation of Neuropeptide F receptor neurons

“…There is considerable anatomical overlap between brain regions that process reward and stress stimuli, as well as opposing functionality: exposure to natural rewards buffers the effect of stressors, while stressors such as social defeat can alter sensitivity to reward and increase the rewarding value of certain addictive drugs [27,[32][33][34][35][36][37][38]. An example of such opposing functions is seen in rodents where corticotropin-releasing factor (CRF) increases alcohol intake, and the binding of Neuropeptide Y (NPY) to NPY receptor Y1 on CRF-positive neurons within the bed nucleus of the stria terminalis (BNST) inhibits binge alcohol drinking [34,39,40].…”