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The prospect of gaining money is an incentive widely at play in the real world. Such monetary motivation might have particularly strong influence when the cognitive system is challenged, such as when needing to process conflicting stimulus inputs. Here, we employed manipulations of reward-prospect and attentional-preparation levels in a cued-Stroop stimulus conflict task, along with the high temporal resolution of electrical brain recordings, to provide insight into the mechanisms by which reward-prospect and attention interact and modulate cognitive task performance. In this task, the cue indicated whether or not the participant needed to prepare for an upcoming Stroop stimulus and, if so, whether there was the potential for monetary reward (dependent on performance on that trial). Both cued attention and cued reward-prospect enhanced preparatory neural activity, as reflected by increases in the hallmark attention-related negative-polarity ERP slow wave (contingent negative variation [CNV]) and reductions in oscillatory Alpha activity, which was followed by enhanced processing of the subsequent Stroop stimulus. In addition, similar modulations of preparatory neural activity (larger CNVs and reduced Alpha) predicted shorter versus longer response times (RTs) to the subsequent target stimulus, consistent with such modulations reflecting trial-to-trial variations in attention. Particularly striking were the individual differences in the utilization of reward-prospect information. In particular, the size of the reward effects on the preparatory neural activity correlated across participants with the degree to which reward-prospect both facilitated overall task performance (shorter RTs) and reduced conflict-related behavioral interference. Thus, the prospect of reward appears to recruit attentional preparation circuits to enhance processing of task-relevant target information.

The contingent negative variation, a slow cortical potential, occurs when humans are warned by a stimulus about an upcoming task. The cognitive processes that give rise to this EEG potential are not yet well understood. To explain these processes, we adopt a recently developed theoretical framework from the area of perceptual decision-making. This framework assumes that the basal ganglia control the tradeoff between fast and accurate decision-making in the cortex. It suggests that an increase in cortical excitability serves to lower response caution, which results in faster but more error prone responding. We propose that the CNV reflects this increased cortical excitability. To test this hypothesis, we conducted an EEG experiment in which participants performed the random dot motion task either under speed or under accuracy stress. Our results show that trial-by-trial fluctuations in participants' response speed as well as model-based estimates of response caution correlated with single-trial CNV amplitude under conditions of speed but not accuracy stress. We conclude that the CNV might reflect adjustments of response caution, which serves to enhance quick decision-making. •A neurophysiological model of decision-making is applied to EEG data.•Single-trial estimates of speed-accuracy tradeoff are correlated with EEG data.•Contingent negative variation reflects the setting of the speed-accuracy tradeoff.•Speed-accuracy tradeoff is set before the decision process.

In schizophrenia patients, glutathione dysregulation at the gene, protein and functional levels, leads to N -methyl- D -aspartate (NMDA) receptor hypofunction. These patients also exhibit deficits in auditory sensory processing that manifests as impaired mismatch negativity (MMN), which is an auditory evoked potential (AEP) component related to NMDA receptor function. N -acetyl-cysteine (NAC), a glutathione precursor, was administered to patients to determine whether increased levels of brain glutathione would improve MMN and by extension NMDA function. A randomized, double-blind, cross-over protocol was conducted, entailing the administration of NAC (2g/day) for 60 days and then placebo for another 60 days (or vice versa). 128-channel AEPs were recorded during a frequency oddball discrimination task at protocol onset, at the point of cross-over, and at the end of the study. At the onset of the protocol, the MMN of patients was significantly impaired compared to sex- and age- matched healthy controls ( p =0.003), without any evidence of concomitant P300 component deficits. Treatment with NAC significantly improved MMN generation compared with placebo ( p =0.025) without any measurable effects on the P300 component. MMN improvement was observed in the absence of robust changes in assessments of clinical severity, though the latter was observed in a larger and more prolonged clinical study. This pattern suggests that MMN enhancement may precede changes to indices of clinical severity, highlighting the possible utility AEPs as a biomarker of treatment efficacy. The improvement of this functional marker may indicate an important pathway towards new therapeutic strategies that target glutathione dysregulation in schizophrenia.

Patients with attention deficit-hyperactivity disorder (ADHD) exhibit difficulties in multiple attentional functions. Although high heritability rates suggest a strong genetic impact, aetiological pathways from genes and environmental factors to the ADHD phenotype are not well understood. Tracking the time course of deviant task processing using event-related electrophysiological brain activity should characterize the impact of familiality on the sequence of cognitive functions from preparation to response control in ADHD. Method Preparation and response control were assessed using behavioural and electrophysiological parameters of two versions of a cued continuous performance test with varying attentional load in boys with ADHD combined type (n = 97), their non-affected siblings (n = 27) and control children without a family history of ADHD (n = 43). Children with ADHD and non-affected siblings showed more variable performance and made more omission errors than controls. The preparatory Cue-P3 and contingent negative variation (CNV) following cues were reduced in both ADHD children and their non-affected siblings compared with controls. The NoGo-P3 was diminished in ADHD compared with controls whilst non-affected siblings were located intermediate but did not differ from both other groups. No clear familiality effects were found for the Go-P3. Better task performance was further associated with higher CNV and P3 amplitudes. Impairments in performance and electrophysiological parameters reflecting preparatory processes and to some extend also for inhibitory response control, especially under high attentional load, appeared to be familially driven in ADHD and may thus constitute functionally relevant endophenotypes for the disorder.

RationaleCue avoidance training (CAT) reduces alcohol consumption in the laboratory. However, the neural mechanisms that underlie the effects of this intervention are poorly understood.ObjectivesThe present study investigated the effects of a single session of CAT on event-related and readiness potentials during preparation of approach and avoidance movements to alcohol cues.MethodsHeavy drinking young adults (N = 60) were randomly assigned to complete either CAT or control training. After training, we recorded participants’ event-related and motor readiness potentials as they were preparing to respond.ResultsIn the CAT group, N200 amplitude was higher when preparing to approach rather than avoid alcohol pictures. In the control group, N200 amplitudes did not differ for approach and avoidance to alcohol pictures. Regarding the late positive potential (LPP), in the CAT group, the negativity of this was blunted when preparing to avoid alcohol pictures relative to when preparing to avoid control pictures. In the control group, the negativity of the LPP was blunted when preparing to approach alcohol pictures relative to when preparing to approach control pictures. There were no effects on motor readiness potentials. Behavioural effects indicated short-lived effects of training on reaction times during the training block that did not persist when participants were given time to prepare their motor response before executing it during the EEG testing block.ConclusionsAfter a single session of CAT, the enhanced N200 when approaching alcohol cues may indicate the engagement of executive control to overcome the associations learned during training. These findings clarify the neural mechanisms that may underlie the effects of CAT on drinking behaviour.

Background Central information processing, visible in evoked potentials like the contingent negative variation (CNV) is altered in migraine patients who exhibit higher CNV amplitudes and a reduced habituation. Both characteristics were shown to be normalized under different prophylactic migraine treatment options whereas Progressive Muscle Relaxation (PMR) has not yet been examined. We investigated the effect of PMR on clinical course and CNV in migraineurs in a quasi-randomized, controlled trial. Methods Thirty-five migraine patients and 46 healthy controls were examined. Sixteen migraineurs and 21 healthy participants conducted a 6-week PMR-training with CNV-measures before and after as well as three months after PMR-training completion. The remaining participants served as controls. The clinical course was analyzed with two-way analyses of variance (ANOVA) with repeated measures. Pre-treatment CNV differences between migraine patients and healthy controls were examined with t-tests for independent measures. The course of the CNV-parameters was examined with three-way ANOVAs with repeated measures. Results After PMR-training, migraine patients showed a significant reduction of migraine frequency. Preliminary to the PMR-training, migraine patients exhibited higher amplitudes in the early component of the CNV (iCNV) and the overall CNV (oCNV) than healthy controls, but no differences regarding habituation. After completion of the PMR-training, migraineurs showed a normalization of the iCNV amplitude, but neither of the oCNV nor of the habituation coefficient. Conclusions The results confirm clinical efficacy of PMR for migraine prophylaxis. The pre-treatment measure confirms altered cortical information processing in migraine patients. Regarding the changes in the iCNV after PMR-training, central nervous mechanisms of the PMR-effect are supposed which may be mediated by the serotonin metabolism.

Rationale Many studies have reported deficits of mismatch negativity (MMN) in schizophrenic patients. Pharmacological challenges with hallucinogens in healthy humans are used as models for psychotic states. Previous studies reported a significant reduction of MMN after ketamine ( N -methyl- d -aspartate acid [NMDA] antagonist model) but not after psilocybin (5HT 2A agonist model). Objectives The aim of the present study was to directly compare the two models of psychosis using an intraindividual crossover design. Materials and methods Fifteen healthy subjects participated in a randomized, double-blind, crossover study with a low and a high dose of the 5HT 2A agonist dimethyltryptamine (DMT) and the NMDA antagonist S -ketamine. During electroencephalographic recording, the subjects were performing the AX-version of a continuous performance test (AX-CPT). A source analysis of MMN was performed on the basis of a four-source model of MMN generation. Results Nine subjects completed both experimental days with the two doses of both drugs. Overall, we found blunted MMN and performance deficits in the AX-CPT after both drugs. However, the reduction in MMN activity was overall more pronounced after S -ketamine intake, and only S -ketamine had a significant impact on the frontal source of MMN. Conclusions The NDMA antagonist model and the 5HT 2A agonist model of psychosis display distinct neurocognitive profiles. These findings are in line with the view of the two classes of hallucinogens modeling different aspects of psychosis.

Rationale The basal ganglia play an important role in motor control, which is dependent on dopaminergic input. Preparation of a motor response has been associated with dopamine release in the basal ganglia, and response readiness may therefore serve as a pharmacodynamic marker of dopamine activity. Methods We measured response readiness using the amplitude of the contingent negative variation (CNV), a slow negative shift in the electroencephalogram. The CNV is evoked in a paradigm in which a warning stimulus (S1) signals the occurrence of the imperative stimulus (S2) 4 s later, to which the participant has to respond. CNV was assessed in healthy volunteers after administration of placebo or 10, 20 or 40 mg of methylphenidate, a catecholamine re-uptake blocker which primarily enhances the synaptic concentration of dopamine and to a lesser extent also noradrenaline. In addition, participants filled out two visual analogue scales measuring subjective ratings of mood and alertness: Profile of Mood States and Bond and Lader. Results Methylphenidate dose dependently increased CNV amplitude and decreased reaction times. Furthermore, participants reported improved mood, feeling more alert, vigorous and content and less angry and tired after methylphenidate. Conclusions These results indicate that dopamine availability increases response readiness as measured by the CNV paradigm. The CNV appears to be a good candidate biomarker for assessing changes in dopaminergic function by treatments that either directly or indirectly target the dopaminergic system.

Much of human learning happens in the social world. A person’s social identity—the groups to which they belong, the people with whom they identify—is a powerful cue that can affect our goal-directed behaviors, often implicitly. In the present experiment, we explored the underlying neural mechanisms driving these processes, testing hypotheses derived from social identity theory. In a within-subjects design, participants underwent a minimal group manipulation where they were randomly assigned to an arbitrary ingroup. In two blocks of the experiment, participants were asked to complete a task for money while being observed by an ingroup member and outgroup member separately. Results revealed that being observed by an ingroup or outgroup member led to divergent patterns of neural activity associated with feedback monitoring, namely the feedback-related negativity (FRN). Receiving feedback in the presence of an ingroup member produced a typical FRN signal, but the FRN was dampened while receiving feedback in the presence of an outgroup member. Further, this differentiated neural pattern was exaggerated in people who reported greater intergroup bias. Together, the mere presence of a person can alter how the brain adaptively monitors feedback, impairing the reinforcement learning signal when the person observing is an outgroup member.

The error-related negativity (ERN) is an event-related potential (ERP) that indexes error monitoring. Research suggests that the ERN is increased in internalizing disorders, such as depression and anxiety. Although studies indicate that the ERN is insensitive to state-related fluctuations in anxiety, few studies have carefully examined the effect of state-related changes in sadness on the ERN. In the current study, we sought to determine whether the ERN would be altered by a sad mood induction using a between-subjects design. Additionally, we explored if this relationship would be moderated by individual differences in neuroticism—a personality trait related to both anxiety and depression. Forty-seven undergraduate participants were randomly assigned to either a sad or neutral mood induction prior to performing an arrow version of the flanker task. Participants reported greater sadness following the sad than neutral mood induction; there were no significant group differences on behavioral or ERP measures. Across the entire sample, however, participants with a larger increase in sad mood from baseline to post-induction had a larger (i.e. more negative) ERN. Furthermore, this effect was larger among individuals reporting higher neuroticism. These data indicate that neuroticism moderates the relationship between the ERN and changes in sad mood.