Impaired reward prediction error encoding and striatal-midbrain connectivity in depression.

Anhedonia (hyposensitivity to rewards) and negative bias (hypersensitivity to punishments) are core features of major depressive disorder (MDD), which could stem from abnormal reinforcement learning. Emerging evidence highlights blunted reward learning and reward prediction error (RPE) signaling in the striatum in MDD, although inconsistencies exist. Preclinical studies have clarified that ventral tegmental area (VTA) neurons encode RPE and habenular neurons encode punishment prediction error (PPE), which are then transmitted to the striatum and cortex to guide goal-directed behavior.

Perceived life stress exposure modulates reward-related medial prefrontal cortex responses to acute stress in depression.

Introduction: Major depressive disorder (MDD) is often precipitated by life stress and growing evidence suggests that stress-induced alterations in reward processing may contribute to such risk. However, no human imaging studies have examined how recent life stress exposure modulates the neural systems that underlie reward processing in depressed and healthy individuals.

Methods: In this proof-of-concept study, 12 MDD and 10 psychiatrically healthy individuals were interviewed using the Life Events and Difficulties Schedule (LEDS) to assess their perceived levels of recent acute and chronic life stress exposure.

Decreased cognitive control in response to negative information in patients with remitted depression: an event-related potential study.

Background: Major depressive disorder (MDD) is associated with difficulty disengaging attention from emotionally negative information. Few studies have investigated whether euthymic individuals with a history of depression (remitted MDD [rMDD]) show similar deficits, and little is known about concomitant neurophysiological features of such deficits. To fill these gaps, we investigated cognitive control over emotional stimuli in participants with rMDD and controls without history of depression or psychopathology.

Childhood adversity is associated with left basal ganglia dysfunction during reward anticipation in adulthood.

Background: Childhood adversity increases the risk of psychopathology, but the neurobiological mechanisms underlying this vulnerability are not well-understood. In animal models, early adversity is associated with dysfunction in basal ganglia regions involved in reward processing, but this relationship has not been established in humans.

Methods: Functional magnetic resonance imaging was used to examine basal ganglia responses to: 1) cues signaling possible monetary rewards and losses; and 2) delivery of monetary gains and penalties, in 13 young adults who experienced maltreatment before age 14 years and 31 nonmaltreated control subjects.

Cortisol response to interpersonal stress in young adults with borderline personality disorder: a pilot study.

Hypothalamic-pituitary-adrenal axis dysregulation after stress was found to be associated with borderline personality disorder (BPD). Nine female BPD young adults and 12 control subjects were investigated for stress reactivity and recovery after an interpersonal conflict discussion with their mothers. BPD subjects showed a delayed cortisol response after psychosocial stress.