Objective: Patients with major depressive disorder tend to exhibit poorer decision-making capacity than the general population, but neurobiological evidence is lacking. Functional near-infrared spectroscopy monitors changes in oxy-haemoglobin concentration in the cerebral cortex. It may provide an objective assessment of neurophysiological responses during decision-making processes. Thus, this study investigated the effect of major depressive disorder diagnosis and severity on prefrontal cortex activity during the Iowa gambling task. Methods: Right-handed healthy controls ( n = 25) and patients with major depressive disorder ( n = 25) were matched for age, gender, ethnicity and years of education in this cross-sectional study. Functional near-infrared spectroscopy signals and the responses made during a computerised Iowa gambling task were recorded. In addition, demographics, clinical history and symptom severity were noted. Results: Compared to healthy controls, patients with major depressive disorder had reduced haemodynamic response in several cortical regions of the frontal lobe (Hedge’s g range from 0.71 to 1.52; p values range from ⩽0.001 to 0.041). Among patients, mean oxy-haemoglobin declined with major depressive disorder severity in the right orbitofrontal cortex (Pearson’s r = −0.423; p = 0.024). Conclusion: Haemodynamic dysfunction of the prefrontal cortex during decision-making processes is associated with major depressive disorder diagnosis and severity. These neurophysiological alterations may have a role in the decision-making capacity of patients with major depressive disorder.

cues associated with either a high or low electrical pain for 20 times each. In the testing stage, the high cue, low cue, and a new cue were all paired with identical moderate pain for 20 times each. In study 2, a verbal suggestion plus conditioning paradigm was used. Three identical inert ointments were applied to 3 sites on each participant's forearm, with the sites randomized across participants. A female experimenter described ointments as creams that increase pain (nocebo), reduce pain (placebo), and have no effect on pain (control), respectively. After 10 min, the 3 sites were stimulated for 10 times with high, moderate, and low shocks, corresponding to their instructed functions, to strengthen the effect of verbal suggestions. In the subsequent testing stage, all 3 sites were paired with moderate shocks for 20 times each.Participants rated how much pain they felt after each shock, using the same 9-point numeric rating scale. The placebo and nocebo effects were assessed as participants rated the low-cue (study 1) or placebo site (study 2)-associated shock as less painful and high-cue/nocebo site-associated shock as more painful compared to the new-cue/control site-associated shock during the test stage.Data from 12 participants were excluded because of poor pain discrimination during calibration or doubt of ointments' effects, leaving 306 participants for analysis (age, 18-26 years). A 2 (group: oxytocin/saline) × 2 (dosage: 24/40 IU) factorial ANOVA on placebo effect revealed no main effects and interaction effect in both studies (study 1: group, F(1, 156) = 0.16, p = 0.692; dosage, F(1, 156) = 0.06, p = 0.814; group × dosage, F(1, 156) = 0.30, p = 0.588; study 2: group, F(1, 142) = 0.17, p = 0.682; dosage, F(1, 142) = 0.03, p = 0.860; group × dosage, F(1, 142) = 0.09, p = 0.764). A similar ANOVA on nocebo effect also revealed no main effects and interaction effect (study 1: group, F(1, 156) = 0.29, p = 0.589; dosage, F(1, 156) = 0.65, p = 0.420; group × dosage, F(1, 156) = 1.12, p = 0.292; study 2: group, F(1, 142) < 0.001, p = 0.99; dosage, F(1, 142) = 0.57, p = 0.452; group × dosage, F(1, 142) = 0.98, p = 0.324).To further examine whether sex modulates the effect of oxytocin on placebo and nocebo effects, we conducted a 2 (group: oxytocin/ saline) × 2 (dosage: 24/40 IU) × 2 (sex: female/male) factorial ANOVA on placebo and nocebo responses, respectively. Results showed no sex-related effects (p values > 0.1), possibly due to the small number of participants in each subgroup for each gender. In addition, we examined pain ratings in the conditioning stage and found no significant differences across 4 arms in both studies (p values > 0.1), suggesting that the strength of conditioning was well-balanced across groups.In summary, using a randomized, double-blind design, we found no evidence for oxytocin effects on placebo and nocebo across paradigms and dosages in a large sample. Our findings challenge previous findings that placebo responses can be enhanced by the application of intranasal oxytocin and furth...

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Background Internet gaming disorder (IGD) is a type of behavioural addictions. One of the key features of addiction is the excessive exposure to addictive objectives (e.g. drugs) reduces the sensitivity of the brain reward system to daily rewards (e.g. money). This is thought to be mediated via the signals expressed as dopaminergic reward prediction error (RPE). Emerging evidence highlights blunted RPE signals in drug addictions. However, no study has examined whether IGD also involves alterations in RPE signals that are observed in other types of addictions. Methods To fill this gap, we used functional magnetic resonance imaging data from 45 IGD and 42 healthy controls (HCs) during a reward-related prediction-error task and utilised a psychophysiological interaction (PPI) analysis to characterise the underlying neural correlates of RPE and related functional connectivity. Results Relative to HCs, IGD individuals showed impaired reinforcement learning, blunted RPE signals in multiple regions of the brain reward system, including the right caudate, left orbitofrontal cortex (OFC), and right dorsolateral prefrontal cortex (DLPFC). Moreover, the PPI analysis revealed a pattern of hyperconnectivity between the right caudate, right putamen, bilateral DLPFC, and right dorsal anterior cingulate cortex (dACC) in the IGD group. Finally, linear regression suggested that the connection between the right DLPFC and right dACC could significantly predict the variation of RPE signals in the left OFC. Conclusions These results highlight disrupted RPE signalling and hyperconnectivity between regions of the brain reward system in IGD. Reinforcement learning deficits may be crucial underlying characteristics of IGD pathophysiology.

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