Patterns of neural activity in response to threatening faces are predictive of autistic traits: modulatory effects of oxytocin receptor genotype.

Autistic individuals generally demonstrate impaired emotion recognition but it is unclear whether effects are emotion-specific or influenced by oxytocin receptor (OXTR) genotype. Here we implemented a dimensional approach using an implicit emotion recognition task together with functional MRI in a large cohort of neurotypical adult participants (N = 255, male = 131, aged 17-29 years) to establish associations between autistic traits and neural and behavioral responses to specific face emotions, together with modulatory effects of OXTR genotype. A searchlight-based multivariate pattern analysis (MVPA) revealed an extensive network of frontal, basal ganglia, cingulate and limbic regions exhibiting significant predictability for autistic traits from patterns of responses to angry relative to neutral expression faces. Functional connectivity analyses revealed a genotype interaction (OXTR SNPs rs2254298, rs2268491) for coupling between the orbitofrontal cortex and mid-cingulate during angry expression processing, with a negative association between coupling and autistic traits in the risk-allele group and a positive one in the non-risk allele group. Overall, results indicate extensive emotion-specific associations primarily between patterns of neural responses to angry faces and autistic traits in regions processing motivation, reward and salience but not in early visual processing. Functional connections between these identified regions were not only associated with autistic traits but also influenced by OXTR genotype. Thus, altered patterns of neural responses to threatening faces may be a potential biomarker for autistic symptoms although modulatory influences of OXTR genotype need to be taken into account.

A brief real-time fNIRS-informed neurofeedback training of the prefrontal cortex changes brain activity and connectivity during subsequent working memory challenge.

Working memory (WM) represents a building-block of higher cognitive functions and a wide range of mental disorders are associated with WM impairments. Initial studies have shown that several sessions of functional near-infrared spectroscopy (fNIRS) informed real-time neurofeedback (NF) allow healthy individuals to volitionally increase activity in the dorsolateral prefrontal cortex (DLPFC), a region critically involved in WM. For the translation to therapeutic or neuroenhancement applications, however, it is critical to assess whether fNIRS-NF success transfers into neural and behavioral WM enhancement in the absence of feedback. We therefore combined single-session fNIRS-NF of the left DLPFC with a randomized sham-controlled design (N = 62 participants) and a subsequent WM challenge with concomitant functional MRI. Over four runs of fNIRS-NF, the left DLPFC NF training group demonstrated enhanced neural activity in this region, reflecting successful acquisition of neural self-regulation. During the subsequent WM challenge, we observed no evidence for performance differences between the training and the sham group. Importantly, however, examination of the fMRI data revealed that - compared to the sham group - the training group exhibited significantly increased regional activity in the bilateral DLPFC and decreased left DLPFC - left anterior insula functional connectivity during the WM challenge. Exploratory analyses revealed a negative association between DLPFC activity and WM reaction times in the NF group. Together, these findings indicate that healthy individuals can learn to volitionally increase left DLPFC activity in a single training session and that the training success translates into WM-related neural activation and connectivity changes in the absence of feedback. This renders fNIRS-NF as a promising and scalable WM intervention approach that could be applied to various mental disorders.

A central serotonin regulating gene polymorphism (TPH2) determines vulnerability to acute tryptophan depletion-induced anxiety and ventromedial prefrontal threat reactivity in healthy young men.

Serotonin (5-HT) has long been implicated in adaptive emotion regulation as well as the development and treatment of emotional dysregulations in mental disorders. Accumulating evidence suggests a genetic vulnerability may render some individuals at a greater risk for the detrimental effects of transient variations in 5-HT signaling. The present study aimed to investigate whether individual variations in the Tryptophan hydroxylase 2 (TPH2) genetics influence susceptibility for behavioral and neural threat reactivity dysregulations during transiently decreased 5-HT signaling. To this end, interactive effects between TPH2 (rs4570625) genotype and acute tryptophan depletion (ATD) on threat reactivity were examined in a within-subject placebo-controlled pharmacological fMRI trial (n = 51). A priori genotype stratification of extreme groups (GG vs. TT) allowed balanced sampling. While no main effects of ATD on neural reactivity to threat-related stimuli and mood state were observed in the entire sample, accounting for TPH2 genotype revealed an ATD-induced increase in subjective anxious arousal in the GG but not the TT carriers. The effects were mirrored on the neural level, such that ATD specifically reduced ventromedial prefrontal cortex reactivity towards threat-related stimuli in the GG carriers. Furthermore, the ATD-induced increase in subjective anxiety positively associated with the extent of ATD-induced changes in ventromedial prefrontal cortex activity in response to threat-related stimuli in GG carriers. Together the present findings suggest for the first time that individual variations in TPH2 genetics render individuals susceptible to the anxiogenic and neural effects of a transient decrease in 5-HT signaling.

Verbal information exchange enhances collective performance through increasing group identification.

Information exchange is a key factor in the attainment of collective outcomes and the navigation of social life. In the current study, we investigated whether and how information exchange enhanced collective performance by combining behavioral and neuroimaging approaches from the perspective of multiparticipant neuroscience. To evaluate collective performance, we measured the collaborative problem-solving abilities of triads working on a murder mystery case. We first found that verbal information exchange significantly enhanced collective performance compared to nonverbal exchange. Moreover, both group sharing and group discussion positively contributed to this effect, with group discussion being more essential. Importantly, group identification mediated the positive effect of verbal information exchange on collective performance. This mediation was supported by higher interactive frequency and enhanced within-group neural synchronization (GNS) in the dorsolateral prefrontal cortex (DLPFC). Taken together, we provided a multiparticipant theoretical model to explain how verbal information exchange enhanced collective performance. Our findings deepen the insight into the workings of group decision-making.

Shared intentionality modulates interpersonal neural synchronization at the establishment of communication system.

Whether and how shared intentionality (SI) influences the establishment of a novel interpersonal communication system is poorly understood. To investigate this issue, we designed a coordinating symbolic communication game (CSCG) and applied behavioral, functional near-infrared spectroscopy (fNIRS)-based hyperscanning, and hyper-transcranial alternating current stimulation (hyper-tACS) methods. Here we show that SI is a strong contributor to communicative accuracy. Moreover, SI, communicative accuracy, and interpersonal neural synchronization (INS) in the right superior temporal gyrus (rSTG) are higher when dyads successfully establish a novel communication system. Furthermore, the SI influences communicative accuracy by increasing INS. Additionally, using time series and long short-term memory neural network analyses, we find that the INS can predict communicative accuracy at the early formation stage of the communication system. Importantly, the INS partially mediates the relationship between the SI and the communicative accuracy only at the formation stage of the communication system. In contrast, when the communication system is established, SI and INS no longer contribute to communicative accuracy. Finally, the hyper-tACS experiment confirms that INS has a causal effect on communicative accuracy. These findings suggest a behavioral and neural mechanism, subserved by the SI and INS, that underlies the establishment of a novel interpersonal communication system.

Functional near-infrared spectroscopy neurofeedback of dorsolateral prefrontal cortex enhances human spatial working memory.

Significance: Spatial working memory (SWM) is essential for daily life and deficits in this domain represent a common impairment across aging and several mental disorders. Impaired SWM has been closely linked to dysregulations in dorsolateral prefrontal cortex (DLPFC) activation. Aim: The present study evaluates the feasibility and maintenance of functional near-infrared spectroscopy neurofeedback (fNIRS-NF) training of the DLPFC to enhance SWM in healthy individuals using a real-time fNIRS-NF platform developed by the authors. Approach: We used a randomized sham-controlled between-subject fNIRS-NF design with 60 healthy subjects as a sample. Training-induced changes in the DLPFC, SWM, and attention performance served as primary outcomes. Results: Feedback from the target channel significantly increased regional-specific DLPFC activation over the fNIRS-NF training compared to sham NF. A significant group difference in NF-induced frontoparietal connectivity was observed. Compared to the control group, the experimental group demonstrated significantly improved SWM and attention performance that were maintained for 1 week. Furthermore, a mediation analysis demonstrated that increased DLPFC activation mediated the effects of fNIRS-NF treatment on better SWM performance. Conclusions: The present results demonstrated that successful self-regulation of DLPFC activation may represent a long-lasting intervention to improve human SWM and has the potential for further applications.

The single- and dual-brain mechanisms underlying the adviser's confidence expression strategy switching during influence management.

Effective influence management during advice-giving requires individuals to express confidence in the advice properly and switch timely between the 'competitive' strategy and the 'defensive' strategy. However, how advisers switch between these two strategies, and whether and why there exist individual differences during this process remain elusive. We used an advice-giving game that manipulated incentive contexts (Incentivized/Non-Incentivized) to induce the adviser's confidence expression strategy switching and measured the brain activities of adviser and advisee concurrently using functional near-infrared spectroscopy (fNIRS). Behaviorally, we observed individual differences in strategy switching. Some advisers applied the 'defensive' strategy when incentivized and the 'competitive' strategy when not incentivized, while others applied the 'competitive' strategy when incentivized and the 'defensive' strategy when not incentivized. This effect was mediated by the adviser's perceived stress in each condition and was reflected by the frequencies of advice-taking in the advisees. Neurally, brain activation in the dorsolateral prefrontal cortex (DLPFC) supported strategy switching, as well as interpersonal neural synchronization (INS) in the temporoparietal junction (TPJ) that supported influence management. This two-in-one process, i.e., confidence expression strategy switching and the corresponding influence management, was linked and modulated by the strength of DLPFC-TPJ functional connectivity in the adviser. We further developed a descriptive model that contributed to understanding the adviser's strategy switching during influence management.

The right inferior frontal gyrus as pivotal node and effective regulator of the basal ganglia-thalamocortical response inhibition circuit.

Background: The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models. However, the pivotal nodes and directed causal regulation within this inhibitory circuit in humans remains controversial. Objective: The main aim of the present study was to determine the causal information flow and critical nodes in the basal ganglia-thalamocortical inhibitory circuits and also to examine whether these are modulated by biological factors (i.e. sex) and behavioral performance. Methods: Here, we capitalize on the recent progress in robust and biologically plausible directed causal modeling (DCM-PEB) and a large response inhibition dataset (n = 250) acquired with concomitant functional magnetic resonance imaging to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP), and thalamus (rThal). Results: The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal. Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal. In addition, sex and performance influenced the functional architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model. Conclusions: Together, these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.

Low threading dislocation density and antiphase boundary free GaAs epitaxially grown on on-axis Si (001) substrates.

Epitaxial growth of III-V materials on a CMOS-compatible Si (001) substrate enables the feasibility of mass production of low-cost and high-yield Si-based III-V optoelectronic devices. However, the material dissimilarities between III-V and group-IV materials induce several types of defects, especially threading dislocations (TDs) and antiphase boundaries (APBs). The presence of these defects is detrimental to the optoelectronic device performance and thus needs to be eliminated. In this paper, the mechanism of APB annihilation during the growth of GaAs on on-axis Si (001) is clarified, along with a detailed investigation of the interaction between TDs and the periodic {110} APBs. A significant reduction in the TD density ascribed to the presence of periodic APBs is discussed. This new observation opens the possibility of reducing both APBs and TDs simultaneously by utilising optimised GaAs growth methods in the future. Hence, a thin APB-free GaAs/Si (001) platform with a low TD density (TDD) was obtained. Based on this platform, a high-performance high-yield III-V optoelectronic device grown on CMOS-compatible Si (001) substrates with an overall thickness below the cracking threshold is feasible, enabling the mass production of Si-based photonic integrated circuits (PICs).

Opposing associations of Internet Use Disorder symptom domains with structural and functional organization of the striatum: A dimensional neuroimaging approach.

Background: Accumulating evidence suggests brain structural and functional alterations in Internet Use Disorder (IUD). However, conclusions are strongly limited due to the retrospective case-control design of the studies, small samples, and the focus on general rather than symptom-specific approaches. Methods: We here employed a dimensional multi-methodical MRI-neuroimaging design in a final sample of n = 203 subjects to examine associations between levels of IUD and its symptom-dimensions (loss of control/time management, craving/social problems) with brain structure, resting state and task-based (pain empathy, affective go/no-go) brain function. Results: Although the present sample covered the entire range of IUD, including normal, problematic as well as pathological levels, general IUD symptom load was not associated with brain structural or functional alterations. However, the symptom-dimensions exhibited opposing associations with the intrinsic and structural organization of the brain, such that loss of control/time management exhibited negative associations with intrinsic striatal networks and hippocampal volume, while craving/social problems exhibited a positive association with intrinsic striatal networks and caudate volume. Conclusions: Our findings provided the first evidence for IUD symptom-domain specific associations with progressive alterations in the intrinsic structural and functional organization of the brain, particularly of striatal systems involved in reward, habitual and cognitive control processes.

Oxytocinergic Modulation of Stress-Associated Amygdala-Hippocampus Pathways in Humans Is Mediated by Serotonergic Mechanisms.

BACKGROUND: The hypothalamic neuropeptide oxytocin (OXT) may exert anxiolytic and stress-reducing actions via modulatory effects on amygdala circuits. Animal models and initial findings in humans suggest that some of these effects are mediated by interactions with other neurotransmitter systems, in particular the serotonin (5-HT) system. Against this background, the present pharmacological resting-state functional magnetic resonance imaging study aimed to determine whether effects of OXT on stress-associated amygdala intrinsic networks are mediated by 5-HT. METHODS: We employed a randomized, placebo-controlled, double-blind parallel-group, pharmacological functional magnetic resonance imaging resting-state experiment with 4 treatment groups in n = 112 healthy male participants. Participants underwent a transient decrease in 5-HT signaling via acute tryptophan depletion (ATD) or a corresponding placebo-control protocol before the administration of intranasal OXT (24 IU) or placebo intranasal spray. RESULTS: OXT and 5-HT modulation exerted interactive effects on the coupling of the left amygdala with the ipsilateral hippocampus and adjacent midbrain. OXT increased intrinsic coupling in this pathway, whereas this effect of OXT was significantly attenuated during transiently decreased central serotonergic signaling induced via acute tryptophan depletion. In the absence of OXT or 5-HT modulation, this pathway showed a trend for an association with self-reported stress perception in everyday life. No interactive effects were observed for the right amygdala. CONCLUSIONS: Together, the findings provide the first evidence, to our knowledge, that the effects of OXT on stress-associated amygdala-hippocampal-midbrain pathways are critically mediated by the 5-HT system in humans.

The mirror neuron system compensates for amygdala dysfunction - associated social deficits in individuals with higher autistic traits.

The amygdala is a core node in the social brain which exhibits structural and functional abnormalities in Autism spectrum disorder and there is evidence that the mirror neuron system (MNS) can functionally compensate for impaired emotion processing following amygdala lesions. In the current study, we employed an fMRI paradigm in 241 subjects investigating MNS and amygdala responses to observation, imagination and imitation of dynamic facial expressions and whether these differed in individuals with higher (n = 77) as opposed to lower (n = 79) autistic traits. Results indicated that individuals with higher compared to lower autistic traits showed worse recognition memory for fearful faces, smaller real-life social networks, and decreased left basolateral amygdala (BLA) responses to imitation. Additionally, functional connectivity between the left BLA and the left inferior frontal gyrus (IFG) as well as some other MNS regions was increased in individuals with higher autistic traits, especially during imitation of fearful expressions. The left BLA-IFG connectivity significantly moderated the autistic group differences on recognition memory for fearful faces, indicating that increased amygdala-MNS connectivity could diminish the social behavioral differences between higher and lower autistic trait groups. Overall, findings demonstrate decreased imitation-related amygdala activity in individuals with higher autistic traits in the context of increased amygdala-MNS connectivity which may functionally compensate for amygdala dysfunction and social deficits. Training targeting the MNS may capitalize on this compensatory mechanism for therapeutic benefits in Autism spectrum disorder.

Sharing Happy Stories Increases Interpersonal Closeness: Interpersonal Brain Synchronization as a Neural Indicator.

Our lives revolve around sharing emotional stories (i.e., happy and sad stories) with other people. Such emotional communication enhances the similarity of story comprehension and neural across speaker-listener pairs. The theory of Emotions as Social Information Model (EASI) suggests that such emotional communication may influence interpersonal closeness. However, few studies have examined speaker-listener interpersonal brain synchronization (IBS) during emotional communication and whether it is associated with meaningful aspects of the speaker-listener interpersonal relationship. Here, one speaker watched emotional videos and communicated the content of the videos to 32 people as listeners (happy/sad/neutral group). Both speaker and listeners' neural activities were recorded using EEG. After listening, we assessed the interpersonal closeness between the speaker and listeners. Compared with the sad group, sharing happy stories showed a better recall quality and a higher rating of interpersonal closeness. The happy group showed higher IBS in the frontal cortex and left temporoparietal cortex than the sad group. The relationship between frontal IBS and interpersonal closeness was moderated by sharing happy/sad stories. Exploratory analysis using support vector regression (SVR) showed that the IBS could also predict the ratings of interpersonal closeness. These results suggest that frontal IBS could serve as an indicator of whether sharing emotional stories facilitate interpersonal closeness. These findings improve our understanding of emotional communication among individuals that guides behaviors during interpersonal interactions.

Segregating domain-general from emotional context-specific inhibitory control systems - ventral striatum and orbitofrontal cortex serve as emotion-cognition integration hubs.

Inhibitory control hierarchically regulates cognitive and emotional systems in the service of adaptive goal-directed behavior across changing task demands and environments. While previous studies convergently determined the contribution of prefrontal-striatal systems to general inhibitory control, findings on the specific circuits that mediate emotional context-specific impact on inhibitory control remained inconclusive. Against this background we combined an evaluated emotional Go/No Go task with fMRI in a large cohort of subjects (N=250) to segregate brain systems and circuits that mediate domain-general from emotion-specific inhibitory control. Particularly during a positive emotional context, behavioral results showed a lower accuracy for No Go trials and a faster response time for Go trials. While the dorsal striatum and lateral frontal regions were involved in inhibitory control irrespective of emotional context, activity in the ventral striatum (VS) and medial orbitofrontal cortex (mOFC) varied as a function of emotional context. On the voxel-wise whole-brain network level, limbic and striatal systems generally exhibited highest changes in global brain connectivity during inhibitory control, while global brain connectivity of the left mOFC was less decreased during emotional contexts. Functional connectivity analyses moreover revealed that negative coupling between the VS with inferior frontal gyrus (IFG)/insula and mOFC varied as a function of emotional context. Together these findings indicate separable domain- general as well as emotional context-specific inhibitory brain systems which specifically encompass the VS and its connections with frontal regions.

Oxytocinergic Modulation of Threat-Specific Amygdala Sensitization in Humans Is Critically Mediated by Serotonergic Mechanisms.

BACKGROUND: Overarching conceptualizations propose that the complex social-emotional effects of oxytocin (OXT) in humans are partly mediated by interactions with other neurotransmitter systems. Recent animal models suggest that the anxiolytic effects of OXT are critically mediated by the serotonin (5-HT) system, yet direct evidence in humans is lacking. METHODS: To determine the role of 5-HT in OXT-induced attenuation of amygdala threat reactivity and sensitization/desensitization, we conducted a parallel-group, randomized, placebo-controlled, double-blind experiment during which 121 healthy subjects underwent a transient decrease in 5-HT signaling via acute tryptophan depletion or the corresponding placebo-control protocol before the administration of intranasal OXT or placebo intranasal spray, respectively. Mean and repetition-dependent changes in threat-specific amygdala reactivity toward threatening stimuli (angry faces) as assessed by functional magnetic resonance imaging served as the primary outcome. RESULTS: No main or interaction effects of treatment on amygdala threat reactivity were observed, yet OXT switched bilateral amygdala threat sensitization to desensitization, and this effect was significantly attenuated during decreased central 5-HT signaling via pretreatment with acute tryptophan depletion. CONCLUSIONS: The present findings provide the first evidence for a role of OXT in threat-specific amygdala desensitization in humans and suggest that these effects are critically mediated by the 5-HT system. OXT may have a therapeutic potential to facilitate amygdala desensitization, and adjunct upregulation of 5-HT neurotransmission may facilitate OXT's anxiolytic potential.

Serotonin and early life stress interact to shape brain architecture and anxious avoidant behavior - a TPH2 imaging genetics approach.

BACKGROUND: Early life stress has been associated with emotional dysregulations and altered architecture of limbic-prefrontal brain systems engaged in emotional processing. Serotonin regulates both, developmental and experience-dependent neuroplasticity in these circuits. Central serotonergic biosynthesis rates are regulated by Tryptophan hydroxylase 2 (TPH2) and transgenic animal models suggest that TPH2-gene associated differences in serotonergic signaling mediate the impact of aversive early life experiences on a phenotype characterized by anxious avoidance. METHODS: The present study employed an imaging genetics approach that capitalized on individual differences in a TPH2 polymorphism (703G/T; rs4570625) to determine whether differences in serotonergic signaling modulate the effects of early life stress on brain structure and function and punishment sensitivity in humans (n = 252). RESULTS: Higher maltreatment exposure before the age of 16 was associated with increased gray matter volumes in a circuitry spanning thalamic-limbic-prefrontal regions and decreased intrinsic communication in limbic-prefrontal circuits selectively in TT carriers. In an independent replication sample, associations between higher early life stress and increased frontal volumes in TT carriers were confirmed. On the phenotype level, the genotype moderated the association between higher early life stress exposure and higher punishment sensitivity. In TT carriers, the association between higher early life stress exposure and punishment sensitivity was critically mediated by increased thalamic-limbic-prefrontal volumes. CONCLUSIONS: The present findings suggest that early life stress shapes the neural organization of the limbic-prefrontal circuits in interaction with individual variations in the TPH2 gene to promote a phenotype characterized by facilitated threat avoidance, thus promoting early adaptation to an adverse environment.

Real-Time Functional Connectivity-Informed Neurofeedback of Amygdala-Frontal Pathways Reduces Anxiety.

BACKGROUND: Deficient emotion regulation and exaggerated anxiety represent a major transdiagnostic psychopathological marker. On the neural level these deficits have been closely linked to impaired, yet treatment-sensitive, prefrontal regulatory control over the amygdala. Gaining direct control over these pathways could therefore provide an innovative and promising intervention to regulate exaggerated anxiety. To this end the current proof-of-concept study evaluated the feasibility, functional relevance and maintenance of a novel connectivity-informed real-time fMRI neurofeedback training. METHODS: In a randomized crossover sham-controlled design, 26 healthy subjects with high anxiety underwent real-time fMRI-guided neurofeedback training to enhance connectivity between the ventrolateral prefrontal cortex (vlPFC) and the amygdala (target pathway) during threat exposure. Maintenance of regulatory control was assessed after 3 days and in the absence of feedback. Training-induced changes in functional connectivity of the target pathway and anxiety ratings served as primary outcomes. RESULTS: Training of the target, yet not the sham control, pathway significantly increased amygdala-vlPFC connectivity and decreased levels of anxiety. Stronger connectivity increases were significantly associated with higher anxiety reduction on the group level. At the follow-up, volitional control over the target pathway was maintained in the absence of feedback. CONCLUSIONS: The present results demonstrate for the first time that successful self-regulation of amygdala-prefrontal top-down regulatory circuits may represent a novel intervention to control anxiety. As such, the present findings underscore both the critical contribution of amygdala-prefrontal circuits to emotion regulation and the therapeutic potential of connectivity-informed real-time neurofeedback.

Functional near-infrared spectroscopy-informed neurofeedback: regional-specific modulation of lateral orbitofrontal activation and cognitive flexibility.

Cognitive flexibility and reward processing critically rely on the orbitofrontal cortex (OFC). Dysregulations in these domains and orbitofrontal activation have been reported in major psychiatric disorders. Hemodynamic brain imaging-informed neurofeedback allows regional-specific control over brain activation and thus may represent an innovative intervention to regulate orbitofrontal dysfunctions. Against this background the present proof-of-concept study evaluates the feasibility and behavioral relevance of functional near-infrared spectroscopy (fNIRS)-assisted neurofeedback training of the lateral orbitofrontal cortex (lOFC). In a randomized sham-controlled between-subject design, 60 healthy participants have undergone four subsequent runs of training to enhance the lOFC activation. Training-induced changes in the lOFC, attentional set-shifting performance, and reward experience have served as primary outcomes. Feedback from the target channel significantly increases the regional-specific lOFC activation over the four training runs in comparison with sham neurofeedback. The real-time OFC neurofeedback group demonstrates a trend for faster responses during the set-shifting relative to the sham neurofeedback group. Within the real-time OFC neurofeedback group, stronger training-induced lOFC increases are associated with higher reward experience. The present results demonstrate that fNIRS-informed neurofeedback allows regional-specific regulation of lOFC activation and may have the potential to modulate the associated behavioral domains. As such fNIRS-informed neurofeedback may represent a promising strategy to regulate OFC dysfunctions in psychiatric disorders.

Internet Communication Disorder and the structure of the human brain: initial insights on WeChat addiction.

WeChat represents one of the most popular smartphone-based applications for communication. Although the application provides several useful features that simplify daily life, a growing number of users spend excessive amounts of time on the application. This may lead to interferences with everyday life and even to addictive patterns of use. In the context of the ongoing discussion on Internet Communication Disorder (ICD), the present study aimed to better characterize the addictive potential of communication applications, using WeChat as an example, by examining associations between individual variations in tendencies towards WeChat addiction and brain structural variations in fronto-striatal-limbic brain regions. To this end levels of addictive tendencies, frequency of use and structural MRI data were assessed in n = 61 healthy participants. Higher tendencies towards WeChat addiction were associated with smaller gray matter volumes of the subgenual anterior cingulate cortex, a key region for monitoring and regulatory control in neural networks underlying addictive behaviors. Moreover, a higher frequency of the paying function was associated with smaller nucleus accumbens volumes. Findings were robust after controlling for levels of anxiety and depression. The present results are in line with previous findings in substance and behavioral addictions, and suggest a similar neurobiological basis in ICD.