Explore the vast range of titles available.

Psychostimulants such as methylphenidate are widely used for their cognitive enhancing effects, but there is large variability in the direction and extent of these effects. We tested the hypothesis that methylphenidate enhances or impairs reward/punishment-based reversal learning depending on baseline striatal dopamine levels and corticostriatal gating of reward/punishment-related representations in stimulus-specific sensory cortex. Young healthy adults (N = 100) were scanned with functional magnetic resonance imaging during a reward/punishment reversal learning task, after intake of methylphenidate or the selective D 2/3 -receptor antagonist sulpiride. Striatal dopamine synthesis capacity was indexed with [ 18 F]DOPA positron emission tomography. Methylphenidate improved and sulpiride decreased overall accuracy and response speed. Both drugs boosted reward versus punishment learning signals to a greater degree in participants with higher dopamine synthesis capacity. By contrast, striatal and stimulus-specific sensory surprise signals were boosted in participants with lower dopamine synthesis. These results unravel the mechanisms by which methylphenidate gates both attention and reward learning. The mechanisms underpinning the variability in methylphenidate’s effects on cognition remain unclear. Here, the authors show that such effects reflect changes in striatal dopamine-related output gating of task-relevant cortical signals, and that these changes depend on baseline dopamine synthesis capacity.

Individual differences in striatal dopamine synthesis capacity have been associated with working memory capacity, trait impulsivity, and spontaneous eye-blink rate (sEBR), as measured with readily available and easily administered, ‘off-the-shelf’ tests. Such findings have raised the suggestion that individual variation in dopamine synthesis capacity, estimated with expensive and invasive brain positron emission tomography (PET) scans, can be approximated with simple, more pragmatic tests. However, direct evidence for the relationship between these simple trait measures and striatal dopamine synthesis capacity has been limited and inconclusive. We measured striatal dopamine synthesis capacity using [ 18 F]-FDOPA PET in a large sample of healthy volunteers (N = 94) and assessed the correlation with simple, short tests of working memory capacity, trait impulsivity, and sEBR. We additionally explored the relationship with an index of subjective reward sensitivity. None of these trait measures correlated significantly with striatal dopamine synthesis capacity, nor did they have out-of-sample predictive power. Bayes factor analyses indicated the evidence was in favour of absence of correlations for all but subjective reward sensitivity. These results warrant caution for using these off-the-shelf trait measures as proxies of striatal dopamine synthesis capacity.

The cognitive enhancing effects of methylphenidate are well established, but the mechanisms remain unclear. We recently demonstrated that methylphenidate boosts cognitive motivation by enhancing the weight on the benefits of a cognitive task in a manner that depended on striatal dopamine. Here, we considered the complementary hypothesis that methylphenidate might also act by changing the weight on the opportunity cost of a cognitive task, that is, the cost of foregoing alternative opportunity. To this end, 50 healthy participants (25 women) completed a novel cognitive effort-discounting task that required choices between task and leisure. They were tested on methylphenidate, placebo, as well as the selective D2-receptor agent sulpiride, the latter to strengthen inference about dopamine receptor selectivity of methylphenidate’s effects. Furthermore, they also underwent an [18F]DOPA PET scan to quantify striatal dopamine synthesis capacity. Methylphenidate boosted choices of cognitive effort over leisure across the group, and this effect was greatest in participants with more striatal dopamine synthesis capacity. The effects of sulpiride did not reach significance. This study strengthens the motivational account of methylphenidate’s effects on cognition, and suggests that methylphenidate reduces the cost of mental labor by increasing striatal dopamine.

RationaleWe constantly need to decide not only which actions to perform, but also how vigorously to perform them. In agreement with an earlier theoretical model, it has been shown that a significant portion of the variance in our action vigor can be explained by the average rate of rewards received for that action. Moreover, this invigorating effect of average reward rate was shown to vary with within-subject changes in dopamine, both in human individuals and experimental rodents.ObjectivesHere, we assessed whether individual differences in the effect of average reward rate on vigor are related to individual variation in a stable measure of striatal dopamine function in healthy, unmedicated participants.MethodsForty-four participants performed a discrimination task to test the effect of average reward rate on response times to index vigor and completed an [18F]-DOPA PET scan to index striatal dopamine synthesis capacity.ResultsWe did not find an interaction between dopamine synthesis capacity and average reward rate across the entire group. However, a post hoc analysis revealed that participants with higher striatal dopamine synthesis capacity, particularly in the nucleus accumbens, exhibited a stronger invigorating effect of average reward rate among the 30 slowest participants.ConclusionsOur findings provide converging evidence for a role of striatal dopamine in average reward rate signaling, thereby extending the current literature on the mechanistic link between average reward rate, vigor, and dopamine.

Reward motivation is known to enhance cognitive control. However, detrimental effects have also been observed, which have been attributed to overdosing of already high baseline dopamine levels by further dopamine increases elicited by reward cues. Aarts et al. (2014) indeed demonstrated, in 14 individuals, that reward effects depended on striatal dopamine synthesis capacity, measured with [ 18 F]FMT-PET: promised reward improved Stroop control in low-dopamine individuals, while impairing it in high-dopamine individuals. Here, we aimed to assess this same effect in 44 new participants, who had previously undergone an [ 18 F]DOPA-PET scan to quantify dopamine synthesis capacity. This sample performed the exact same rewarded Stroop paradigm as in the prior study. However, we did not find any correlation between reward effects on cognitive control and striatal dopamine synthesis capacity. Critical differences between the radiotracers [ 18 F]DOPA and [ 18 F]FMT are discussed, as the discrepancy between the current and our previous findings might reflect the use of the potentially less sensitive [ 18 F]DOPA radiotracer in the current study.

Criminal behaviour poses a big challenge for society. A thorough understanding of the neurobiological mechanisms underlying criminality could optimize its prevention and management. Specifically,elucidating the neural mechanisms underpinning reward expectation might be pivotal to understanding criminal behaviour. So far no study has assessed reward expectation and its mechanisms in a criminal sample. To fill this gap, we assessed reward expectation in incarcerated, psychopathic criminals. We compared this group to two groups of non-criminal individuals: one with high levels and another with low levels of impulsive/antisocial traits. Functional magnetic resonance imaging was used to quantify neural responses to reward expectancy. Psychophysiological interaction analyses were performed to examine differences in functional connectivity patterns of reward-related regions. The data suggest that overt criminality is characterized, not by abnormal reward expectation per se , but rather by enhanced communication between reward-related striatal regions and frontal brain regions. We establish that incarcerated psychopathic criminals can be dissociated from non-criminal individuals with comparable impulsive/antisocial personality tendencies based on the degree to which reward-related brain regions interact with brain regions that control behaviour. The present results help us understand why some people act according to their impulsive/antisocial personality while others are able to behave adaptively despite reward-related urges.

Resting-state studies in depressed patients have revealed increased connectivity within the default mode network (DMN) and task-positive network (TPN). This has been associated with heightened rumination, which is the tendency to repetitively think about symptoms of distress. Here, we performed a pharmacological neuroimaging study in healthy volunteers to investigate whether short-term antidepressant administration could reduce DMN connectivity. We recorded resting-state functional magnetic resonance imaging (fMRI) scans in twenty-three healthy volunteers after two week intake of the combined serotonin–norepinephrine reuptake inhibitor (SNRI) duloxetine in a double-blind, placebo-controlled, crossover study. Duloxetine improved mood in part as a result of increased resilience to the mood-worsening effects of scanning and reduced DMN and TPN connectivity. Within the DMN, duloxetine reduced connectivity between the medial prefrontal cortex (MPFC) and the lateral parietal cortex (LPC) and uncoupled the MPFC from the dorsolateral prefrontal cortex (DLPFC). Within the TPN, duloxetine uncoupled the intraparietal sulcus (IPS) from the inferior occipital gyrus. These results show that two-week antidepressant administration reduces DMN and TPN connectivity in healthy volunteers, which may contribute to their antidepressant effects in depression. •Depressed patients show altered default mode network (DMN) connectivity.•The influence of antidepressants on resting-state connectivity was investigated.•Two week intake of duloxetine reduced DMN and task-positive network connectivity.•Antidepressants may exert their effects by reducing resting-state connectivity.

Current empirical understanding of the relationship between psychopathology and terrorist behaviours in women is limited, because most research focuses on male perpetrators and relies on secondary sources. Addressing this gap is crucial, particularly given previous research that highlights significant differences in mental health problems between women and men involved in non-terrorist violent activities. To empirically examine the presence of psychopathology in women exhibiting terrorist behaviours, as well as its potential role in these behaviours. A case series study of 14 Dutch female convicts associated with the (so-called) Islamic State of Iraq and Syria (ISIS), examining the occurrence and types of mental disorders, psychopathological problems and pathological personality traits, and exploring their potential role in terrorist behaviours based on forensic mental health reports from psychiatrists and psychologists. Half of the women ( = 7) exhibited mental disorders during terrorist activities, primarily personality disorders. Psychopathological problems included susceptibility to influence (71%, = 10), identity problems (64%, = 9), feelings of inferiority (57%, = 8) and naivety (50%, = 7). A significant link between terrorism and mental disorders, psychopathological problems or pathological personality traits was identified in almost half of the women (43%, = 6). Psychopathology is present in some women involved in terrorist behaviours, influencing their involvement, but is absent or irrelevant in others. Identifying psychopathology in women with terrorist tendencies is essential for early prevention and should be a core competency for psychiatrists.

PurposeLow levels of subjective wellbeing in prisoners may relate to mental health problems and difficulties in reintegration after imprisonment. The development of subjective wellbeing during imprisonment is mostly unclear. The purpose of this paper is to explore this development in a longitudinal study in association with mental disorders and socioeconomic factors.Design/methodology/approachSubjective wellbeing was assessed via a visual analogue scale and retrieved at admission to remand prison and then again after four and eight weeks. Changes in subjective wellbeing between time-points were analyzed taking into account mental disorders and socioeconomic factors, which were assessed by use of the Mini International Neuropsychiatric Interview – Plus and the Camberwell Assessment of Need – Forensic Version, respectively.FindingsOn average, subjective wellbeing declined directly after remand prison admission, but differences between individuals were found. At remand prison admission, subjective wellbeing significantly improved rather than declined in prisoners with alcohol and substance use disorders, housing problems, unemployment prior to incarceration and in relatively older prisoners. Other related factors did not add significance to this model. In contrast, during remand imprisonment subjective wellbeing displayed an overall increase. For this increase, no predicting factors were found. However, prisoners with an antisocial personality disorder are more at risk of experiencing a decrease in wellbeing during remand imprisonment.Originality/valueIn general, the Dutch prison system appears not to result in a decrease in subjective wellbeing in prisoners suffering from a mental disorder during remand imprisonment.

Background: Violent offenders with psychopathic tendencies are characterized by instrumental, i.e. planned, callous and unemotional (aggressive) behaviour and have been shown to exhibit abnormal aversive processing. However, the consequences of abnormal aversive processing for instrumental action and associated neural mechanisms are unclear. Methods: Here we address this issue by using event-related functional magnetic resonance imaging in 15 violent offenders with high psychopathic tendencies and 18 matched controls during the performance of an aversive Pavlovian-to-instrumental transfer paradigm. This paradigm allowed us to assess the degree to which aversive Pavlovian cues affect instrumental action and associated neural signaling. Results: Psychopathic tendency scores were associated with an attenuation of aversive Pavlovian inhibition of instrumental action. Moreover, exploratory analyses revealed an anomalous positive association between aversive inhibition of action and aversive inhibition of BOLD signal in the caudate nucleus of violent offenders with psychopathic tendencies. In addition, psychopathic tendency also correlated positively with amygdala reactivity during aversive versus neutral cues in Pavlovian training. Conclusions: These findings strengthen the hypothesis that psychopathic tendencies in violent offenders are related to abnormal impact of aversive processing on instrumental behaviour. The neural effects raise the possibility that this reflects deficient transfer of aversive Pavlovian inhibitory biases onto neural systems that implement instrumental action, including the caudate nucleus.