The effects of psychological stress on approach tendencies for smoking-related cues in smokers.

Stress may potentiate the chronification of nicotine addiction, but the exact mechanisms remain elusive. We performed an explorative pilot study examining the effects of psychological stress, administered via the socially evaluated cold pressor task (SECPT), on implicit approach bias for smoking-related cues in smokers in the approach-avoidance task (AAT). Smokers (N = 24) were subjected to the stress or control condition of the SECPT by using a within-subject design. Consistent with previous findings, a strong approach bias for smoking-related cues in the AAT was found in smokers. Exposure to stress did not affect the general bias for smoking-related cues in the AAT relative to the control condition of the SECPT. In additional explorative analyses, an interaction among carbon monoxide (CO) levels in expired air, cortisol levels, and stress on approach bias for smoking-related cues was found. Higher CO levels, possibly due to recent smoking, prior to stress exposure were associated with an approach bias for smoking-related cues. Our results suggest that CO levels in interaction with stress can modulate implicit, automatic processing in the context of nicotine addiction. Our findings might provide novel cues to how stress influences cigarette craving and smoking behavior.

The role of KIBRA in reconstructive episodic memory.

BACKGROUND: In order to retrieve episodic past events, the missing information needs to be reconstructed using information stored in semantic memory. Failures in these reconstructive processes are expressed as false memories. KIBRA single nucleotide polymorphism (rs17070145) has been linked to episodic memory performance as well as an increased risk of Alzheimer's disease and post-traumatic stress disorder (PTSD). METHODS: Here, the role of KIBRA rs17070145 polymorphism (male and female CC vs. CT/TT carriers) in reconstructive episodic memory in the Deese-Roediger-McDermott (DRM) paradigm was investigated in N = 219 healthy individuals. RESULTS: Female participants outperformed males in the free recall condition. Furthermore, a trend towards a gender x genotype interaction was found for false recognition rates. Female CT/TT carriers exhibited a lower proportion of false recognition rates for associated critical lures as compared to male CT/TT. Additionally, an association between KIBRA rs17070145 genotype, familiarity and recollection based recognition performance was found. In trials with correct recognition of listed items CT/TT carriers showed more "remember", but fewer "know" responses as compared to CC carriers. DISCUSSION AND CONCLUSION: Our findings suggest that the T-allele of KIBRA rs17070145 supports recollection based episodic memory retrieval and contributes to memory accuracy in a gender dependent manner. Findings are discussed in the context of the specific contribution of KIBRA related SNPs to reconstructive episodic memory and its implications for cognitive and emotional symptoms in dementia and PTSD.

The dopamine D2 receptor mediates approach-avoidance tendencies in smokers.

Dopamine D2 receptors (DRD2) have been strongly implicated in reward processing of natural stimuli and drugs. Using the approach-avoidance task (AAT), we recently demonstrated that smokers show an increased approach-bias toward smoking-related cues but not toward naturally rewarding stimuli. Here, we examined the contribution of the DRD2 Taq1B polymorphism to smokers' and non-smokers' responsivity toward smoking versus naturally rewarding stimuli in the AAT. Smokers carrying the minor B1 allele of the DRD2 Taq1B polymorphism showed reduced approach behavior for food-related pictures compared to non-smokers with the same allele. In the group of smokers, a higher approach-bias toward smoking-related compared to food-related pictures was found in carriers of the B1 allele. This pattern was not evident in smokers homozygous for the B2 allele. In addition, smokers with the B1 allele reported fewer attempts to quit smoking relative to smokers homozygous for the B2 allele. This is the first study demonstrating that behavioral shifts in response to smoking relative to natural rewards in smokers are mediated by the DRD2 Taq1B polymorphism. Our results indicate a reduced natural-reward brain reactivity in smokers with a genetically determined decrease in dopaminergic activity (i.e., reduction of DRD2 availability). It remains to be determined whether this pattern might be related to a different outcome after psychological cessation interventions, i.e., AAT modification paradigms, in smokers.

Inactivation of ceramide synthase 6 in mice results in an altered sphingolipid metabolism and behavioral abnormalities.

The N-acyl chain length of ceramides is determined by the specificity of different ceramide synthases (CerS). The CerS family in mammals consists of six members with different substrate specificities and expression patterns. We have generated and characterized a mouse line harboring an enzymatically inactive ceramide synthase 6 (CerS6KO) gene and lacz reporter cDNA coding for ß-galactosidase directed by the CerS6 promoter. These mice display a decrease in C16:0 containing sphingolipids. Relative to wild type tissues the amount of C16:0 containing sphingomyelin in kidney is ∼35%, whereas we find a reduction of C16:0 ceramide content in the small intestine to about 25%. The CerS6KO mice show behavioral abnormalities including a clasping abnormality of their hind limbs and a habituation deficit. LacZ reporter expression in the brain reveals CerS6 expression in hippocampus, cortex, and the Purkinje cell layer of the cerebellum. Using newly developed antibodies that specifically recognize the CerS6 protein we show that the endogenous CerS6 protein is N-glycosylated and expressed in several tissues of mice, mainly kidney, small and large intestine, and brain.

Pathologic and phenotypic alterations in a mouse expressing a connexin47 missense mutation that causes Pelizaeus-Merzbacher-like disease in humans.

Gap junction channels are intercellular conduits that allow diffusional exchange of ions, second messengers, and metabolites. Human oligodendrocytes express the gap junction protein connexin47 (Cx47), which is encoded by the GJC2 gene. The autosomal recessive mutation hCx47M283T causes Pelizaeus-Merzbacher-like disease 1 (PMLD1), a progressive leukodystrophy characterized by hypomyelination, retarded motor development, nystagmus, and spasticity. We introduced the human missense mutation into the orthologous position of the mouse Gjc2 gene and inserted the mCx47M282T coding sequence into the mouse genome via homologous recombination in embryonic stem cells. Three-week-old homozygous Cx47M282T mice displayed impaired rotarod performance but unchanged open-field behavior. 10-15-day-old homozygous Cx47M282T and Cx47 null mice revealed a more than 80% reduction in the number of cells participating in glial networks after biocytin injections into oligodendrocytes in sections of corpus callosum. Homozygous expression of mCx47M282T resulted in reduced MBP expression and astrogliosis in the cerebellum of ten-day-old mice which could also be detected in Cx47 null mice of the same age. Three-month-old homozygous Cx47M282T mice exhibited neither altered open-field behavior nor impaired rotarod performance anymore. Adult mCx47M282T expressing mice did not show substantial myelin alterations, but homozygous Cx47M282T mice, additionally deprived of connexin32, which is also expressed in oligodendrocytes, died within six weeks after birth and displayed severe myelin defects accompanied by astrogliosis and activated microglia. These results strongly suggest that PMLD1 is caused by the loss of Cx47 channel function that results in impaired panglial coupling in white matter tissue.

Reduced speech coherence in psychosis-related social media forum posts.

The extraction of linguistic markers from social media posts, which are indicative of the onset and course of mental disorders, offers great potential for mental healthcare. In the present study, we extracted over one million posts from the popular social media platform Reddit to analyze speech coherence, which reflects formal thought disorder and is a characteristic feature of schizophrenia and associated psychotic disorders. Natural language processing (NLP) models were used to perform an automated quantification of speech coherence. We could demonstrate that users who are active on forums geared towards disorders with a higher degree of psychotic symptoms tend to show a lower level of coherence. The lowest coherence scores were found in users of forums on dissociative identity disorder, schizophrenia, and bipolar disorder. In contrast, a relatively high level of coherence was detected in users of forums related to obsessive-compulsive disorder, anxiety, and depression. Users of forums on posttraumatic stress disorder, autism, and attention-deficit hyperactivity disorder exhibited medium-level coherence. Our findings provide promising first evidence for the possible utility of NLP-based coherence analyses for the early detection and prevention of psychosis on the basis of posts gathered from publicly available social media data. This opens new avenues for large-scale prevention programs aimed at high-risk populations.

Panglial gap junctional communication is essential for maintenance of myelin in the CNS.

In this study, we have investigated the contribution of oligodendrocytic connexin47 (Cx47) and astrocytic Cx30 to panglial gap junctional networks as well as myelin maintenance and function by deletion of both connexin coding DNAs in mice. Biocytin injections revealed complete disruption of oligodendrocyte-to-astrocyte coupling in the white matter of 10- to 15-d-old Cx30/Cx47 double-deficient mice, while oligodendrocyte-to-oligodendrocyte coupling was maintained. There were no quantitative differences regarding cellular networks in acute brain slices obtained from Cx30/Cx47 double-null mice and control littermates, probably caused by the upregulation of oligodendrocytic Cx32 in Cx30/Cx47 double-deficient mice. We observed early onset myelin pathology, and ∼40% of Cx30/Cx47 double-deficient animals died within 42 to 90 d after birth, accompanied by severe motor impairments. Histological and ultrastructural analyses revealed severe vacuolization and myelination defects in all white matter tracts of the CNS. Furthermore, Cx30/Cx47 double-deficient mice exhibited a decreased number of oligodendrocytes, severe astrogliosis, and microglial activation in white matter tracts. Although less affected concerning motor impairment, surviving double-knock-out (KO) mice showed behavioral alterations in the open field and in the rotarod task. Vacuole formation and thinner myelin sheaths were evident also with adult surviving double-KO mice. Since interastrocytic coupling due to Cx43 expression and interoligodendrocytic coupling because of Cx32 expression are still maintained, Cx30/Cx47 double-deficient mice demonstrate the functional role of both connexins for interastrocytic, interoligodendrocytic, and panglial coupling, and show that both connexins are required for maintenance of myelin.

Ablation of neuronal ceramide synthase 1 in mice decreases ganglioside levels and expression of myelin-associated glycoprotein in oligodendrocytes.

Ceramide synthase 1 (CerS1) catalyzes the synthesis of C18 ceramide and is mainly expressed in the brain. Custom-made antibodies to a peptide from the C-terminal region of the mouse CerS1 protein yielded specific immunosignals in neurons but no other cell types of wild type brain, but the CerS1 protein was not detected in CerS1-deficient mouse brains. To elucidate the biological function of CerS1-derived sphingolipids in the brain, we generated CerS1-deficient mice by introducing a targeted mutation into the coding region of the cers1 gene. General deficiency of CerS1 in mice caused a foliation defect, progressive shrinkage, and neuronal apoptosis in the cerebellum. Mass spectrometric analyses revealed up to 60% decreased levels of gangliosides in cerebellum and forebrain. Expression of myelin-associated glycoprotein was also decreased by about 60% in cerebellum and forebrain, suggesting that interaction and stabilization of oligodendrocytic myelin-associated glycoprotein by neuronal gangliosides is due to the C18 acyl membrane anchor of CerS1-derived precursor ceramides. A behavioral analysis of CerS1-deficient mice yielded functional deficits including impaired exploration of novel objects, locomotion, and motor coordination. Our results reveal an essential function of CerS1-derived ceramide in the regulation of cerebellar development and neurodevelopmentally regulated behavior.

Superior working memory and behavioural habituation but diminished psychomotor coordination in mice lacking the ecto-5'-nucleotidase (CD73) gene.

Adenosine is an important neuromodulator in the central nervous system involved in the regulation of wakefulness, sleep, learning and memory, fear and anxiety as well as motor functions. Extracellular adenosine is synthesized by the cell-surface ectoenzyme ecto-5'-nucleotidase (CD73) from 5'-adenosine monophosphate. While CD73 is widely expressed throughout the mammalian brain, its specific role for behaviour is poorly understood. We examined spatial working memory, emotional responses, motor coordination and motor learning as well as behavioural habituation in mice with a targeted deletion of CD73. CD73 knockout (CD73-/-) mice exhibit enhanced spatial working memory in the Y-maze and enhanced long-term behavioural habituation in the open field. Furthermore, impaired psychomotor coordination on the accelerating rotarod was found in CD73-/- mice. No changes in motor learning and/or anxiety-like behaviour were evident in CD73-/- mice. Our data provide evidence for a role of CD73 in the regulation of learning and memory and psychomotor coordination. Our results might be important for the evaluation of adenosine neuromodulators as possible treatments to ameliorate cognitive and motor deficits associated with neurodegenerative diseases.

Generalization of beneficial exposure effects to untreated stimuli from another fear category.

Previous research has shown that fear associated with one stimulus often spreads to other stimuli with similar perceptual features as well as across different stimulus categories. Exposure is considered as the most effective intervention to attenuate exaggerated fear. The extent to which exposure treatment effects can generalize to fears not targeted during treatment remains elusive. Previous studies on possible generalization of beneficial effects of exposure used stimuli sharing the same stimulus category and/or stimuli having high perceptual similarity. The current study examined whether exposure treatment generalization can be achieved for untreated stimuli which do not share any perceptual resemblance and belong to a different fear category. An analogue sample of fifty participants with fear of spiders (animal-related fears) and heights (natural environment-related fears) was tested. Participants have been randomly assigned to either an exposure treatment (n = 24) or a control condition (n = 26). Exposure treatment was designed to only target participants' fear of spiders, leaving their fear of heights untreated. Results demonstrated that the effects of exposure treatment generalized to fear of heights, as indicated by a reduction in behavioral avoidance, as well as self-reported acrophobia symptoms. The present study confutes the assumption that generalization of exposure effects to untreated fears is based on perceptual similarity. Clearly, further research is required to determine the decisive factors, in order to expand the generalization effect permanently to any given type of fear.

The role of self-efficacy in specific fears.

Low self-efficacy for threatening stimuli and situations has been proposed as an important etiological factor in the development and maintenance of specific phobias. The present study examined the relationships between general self-efficacy (GSE), specific self-efficacy (SSE) and specific fears in a representative sample (n = 717). While GSE was associated with higher self-reported fear and avoidance, SSE (e.g. SSE in the presence of animal-related fear) was more related to specific fears. SSE turned out to be a significant predictor of specific fear even after controlling for trait anxiety, age and gender. Interestingly, the association between SSE and specific fear differed across the different fear categories. Fear and avoidance of blood/injection/injuries showed the highest associations with SSE. In contrast, the association between natural environment-related fear and avoidance and GSE or SSE together was only modest. Exploratory analyses revealed a gender-specific effect on the strength of the association between SSE and specific fears. Women scored higher in animal-related fears and SSE. Our findings support the self-efficacy hypothesis of anxiety disorder development and provide a more detailed insight into the role of GSE and SSE in specific fears and phobias.

A fatal alliance: Glial connexins, myelin pathology and mental disorders.

Mature oligodendrocytes are myelin forming glial cells which are responsible for myelination of neuronal axons in the white matter of the central nervous system. Myelin pathology is a major feature of severe neurological disorders. Oligodendrocyte-specific gene mutations and/or white matter alterations have also been addressed in a variety of mental disorders. Breakdown of myelin integrity and demyelination is associated with severe symptoms, including impairments in motor coordination, breathing, dysarthria, perception (vision and hearing), and cognition. Furthermore, there is evidence indicating that myelin sheath defects and white matter pathology contributes to the affective and cognitive symptoms of patients with mental disorders. Oligodendrocytes express the connexins GJC2; mCx47 [human (GJC2) and mouse (mCx47) connexin gene nomenclature according to Söhl and Willecke (2003)], GJB1; mCx32, and GJD1; mCx29 in both white and gray matter. Preclinical findings indicate that alterations in connexin expression in oligodendrocytes and astrocytes can induce myelin defects. GJC2; mCx47 is expressed at early embryonic stages in oligodendrocyte precursors cells which precedes central nervous system myelination. In adult humans and animals GJC2, respectively mCx47 expression is essential for oligodendrocyte function and ensures adequate myelination as well as myelin maintenance in the central nervous system. In the past decade, evidence has accumulated suggesting that mental disorders can be accompanied by changes in connexin expression, myelin sheath defects and corresponding white matter alterations. This dual pathology could compromise inter-neuronal information transfer, processing and communication and eventually contribute to behavioral, sensory-motor, affective and cognitive symptoms in patients with mental disorders. The induction of myelin repair and remyelination in the central nervous system of patients with mental disorders could help to restore normal neuronal information propagation and ameliorate behavioral and cognitive symptoms in individuals with mental disorders.

Conscious knowledge of CS-UCS contingency information affects extinction retrieval of conditioned disgust responses: Findings from an online de novo disgust conditioning task.

Objective: The present study aimed to establish and develop an online de novo conditioning paradigm for the measurement of conditioned disgust responses. We further explored the effects of explicit instructions about the CS-UCS contingency on extinction learning and retrieval of conditioned disgust responses. Method: The study included a sample of 115 healthy participants. Geometric figures served as conditioned stimuli (CS) and disgust-evoking pictures as unconditioned stimuli (UCS). During disgust conditioning, the CS+ was paired with the UCS (66% reinforcement) and the CS- remained unpaired; during extinction and retrieval, no UCS was presented. Half of the participants (n = 54) received instructions prior to the disgust extinction stating that the UCS will not be presented anymore. 1-2 days or 7-8 days later participants performed a retrieval test. CS-UCS contingency, disgust and valence ratings were used as dependent measures. Results: Successful acquisition of conditioned disgust response was observed on the level of CS-UCS contingency, disgust and valence ratings. While some decline in valence and disgust ratings during the extinction stage was observed, contingency instructions did not significantly affect extinction performance. Retrieval one week later revealed that contingency instructions increased the discrimination of the CSs. Conclusions: Extinction of conditioned disgust responses is not affected by explicit knowledge of the CS-UCS contingencies. However, contingency instructions prior to extinction seem to have a detrimental effect on long-term extinction retrieval.

Do oral contraceptives modulate the effects of stress induction on one-session exposure efficacy and generalization in women?

RATIONALE: The administration of glucocorticoids (GC) as an adjunct to exposure represents a promising strategy to improve one-session exposure outcome in anxiety disorders. It remains to be determined whether similar effects can be induced with the use of acute stress. Furthermore, the possible modulation of exposure effects by hormonal factors (e.g., use of oral contraceptives (OCs)) was not explored so far. OBJECTIVES: We investigated whether acute stress prior to one-session exposure for spider fear affects its efficacy in women using oral contraceptives (OC) relative to free-cycling (FC) women. In addition, effects of stress on generalization of exposure therapy effects towards untreated stimuli were examined. METHODS: Women with fears of spiders and cockroaches were randomly assigned to a Stress (n = 24) or No-Stress (n = 24) condition prior to one-session exposure. Of these 48 participants, 19 women used OC (n = 9 in the Stress, and n = 10 in the No-Stress group). All FC women had a regular menstrual cycle and were tested only in the follicular phase of their menstrual cycle. Pre-exposure stress induction was realized with the socially evaluated cold-pressor test. Exposure-induced changes towards treated and untreated fear stimuli were tested with behavioral approach tests for spiders and cockroaches and subjective fear and self-report measures. RESULTS: Acute stress did not influence exposure-induced reduction in fear and avoidance of the treated stimuli (spiders). Similarly, stress had no effect on the generalization of exposure-therapy effects towards untreated stimuli (cockroaches). Exposure-induced reduction in subjective fear and self-report measures for treated stimuli was less evident in women using OC specifically after pre-exposure stress. Women using OC had higher levels of subjective fear and scored higher in self-report measures at post-treatment (24 h after exposure) and follow-up (4 weeks after exposure). CONCLUSIONS: OC intake may represent an important confounding factor in augmentation studies using stress or GC.

Changes in object recognition and anxiety-like behaviour in mice expressing a Cx47 mutation that causes Pelizaeus-Merzbacher-like disease.

Pelizaeus-Merzbacher-like disease is characterized by impaired psychomotor development, ataxia, progressive spasticity and mental retardation. It is induced by mutations in the gap junction gene GJC2 that encodes for the gap junction protein connexin 47. Mice bearing a human Cx47M283T missense mutation have been generated as a transgenic mouse model of Pelizaeus-Merzbacher-like disease. Homozygous expression of the mutant connexin 47 gene in oligodendrocytes resulted in a complex and variable neuropathologic phenotype, which was associated with impairments in motor coordination in juvenile, but not adult mice. In the present study, we have investigated anxiety-like behaviour and spatial working memory in juvenile (P23) and adult (3-month-old) Cx47M282T mutant mice. Adult Cx47M282T mice were also evaluated in terms of neuromotor functions and in the novel object recognition test. Juvenile Cx47M282T mutant mice exhibited an increase in anxiety-like behaviour in the open field test, but no changes in spatial working memory performance. No significant changes in anxiety-like behaviour, spatial working memory or neuromotor functions were observed in the adult Cx47M282T mutant mice. However, novel object recognition was significantly impaired in adult Cx47M282T mice. Our results suggest that the expression of the human Cx47M282T mutation in the mouse causes changes in anxiety-like behaviour in juvenile and novel object recognition impairments in adult mice. It appears that the distortion of panglial gap junction coupling in white and grey matter tissue in the Cx47M282T mice is associated with a complex age-dependent behavioural phenotype including changes in psychomotor, emotional and memory functions.

Towards an animal model of consciousness based on the platform theory.

The evolution of intellectual capacities has brought forth a continuum of consciousness levels subserved by neuronal networks of varying complexity. Brain pathologies, neurodegenerative, and mental diseases affect conscious cognition and behavior. Although impairments in consciousness are among the most devastating consequences of neurological and mental diseases, valid and reliable animal models of consciousness, that could be used for preclinical research are missing. The platform theory holds that the brain enters a conscious operation mode, whenever mental representations of stimuli, associations, concepts, memories, and experiences are effortfully maintained (in working memory) and actively manipulated. We used the platform theory as a framework and evaluation standard to categorize behavioral paradigms with respect to the level of consciousness involved in task performance. According to the platform theory, a behavioral paradigm involves conscious cognitive operations, when the problem posed is unexpected, novel or requires the maintenance and manipulation of a large amount of information to perform cognitive operations on them. Conscious cognitive operations are associated with a relocation of processing resources and the redirection of attentional focus. A consciousness behavioral test battery is proposed that is composed of tests which are assumed to require higher levels of consciousness as compared to other tasks and paradigms. The consciousness test battery for rodents includes the following tests: Working memory in the radial arm maze, episodic-like memory, prospective memory, detour test, and operant conditioning with concurrent variable-interval variable-ratio schedules. Performance in this test battery can be contrasted with the performance in paradigms and tests that require lower levels of consciousness. Additionally, a second more comprehensive behavioral test battery is proposed to control for behavioral phenotypes not related to consciousness. Our theory could serve as a guidance for the decryption of the neurobiological basis of consciousness.

A new path to mental disorders: Through gap junction channels and hemichannels.

Behavioral disturbances related to emotional regulation, reward processing, cognition, sleep-wake regulation and activity/movement represent core symptoms of most common mental disorders. Increasing empirical and theoretical evidence suggests that normal functioning of these behavioral domains relies on fine graded coordination of neural and glial networks which are maintained and modulated by intercellular gap junction channels and unapposed pannexin or connexin hemichannels. Dysfunctions in these networks might contribute to the development and maintenance of psychopathological and neurobiological features associated with mental disorders. Here we review and discuss the evidence indicating a prominent role of gap junction channel and hemichannel dysfunction in core symptoms of mental disorders. We further discuss how the increasing knowledge on intercellular gap junction channels and unapposed pannexin or connexin hemichannels in the brain might lead to deeper mechanistic insight in common mental disorders and to the development of novel treatment approaches. We further attempt to exemplify what type of future research on this topic could be integrated into multidimensional approaches to understand and cure mental disorders.

Recognition memory, primacy vs. recency effects, and time perception in the online version of the fear of scream paradigm.

Anxiety disorders are characterized by cognitive dysfunctions which contribute to the patient's profound disabilities. The threat of shock paradigm represents a validated psychopathological model of anxiety to measure the impact of anxiety on cognitive processes. We have developed an online version of the threat of scream paradigm (ToSP) to investigate the impact of experimental anxiety on recognition memory. Two animated passive walkthrough videos (either under threat of scream or safety conditions) were shown to healthy participants. Recognition memory, primacy vs. recency effects, and subjective estimations of the length of encoding sessions were assessed. Subjective anxiety, stress, and emotional arousal ratings indicated that experimental anxiety could successfully be induced (Safe-Threat) or reversed (Threat-Safe) between the two passive walkthrough sessions. Participants exposed to distress screams showed impaired retrieval of complex information that has been presented in an animated environment. In the threat condition, participants failed to recognize details related to the persons encountered, their spatial locations, as well as information about the temporal order and sequence of encounters. Participant groups, which received a threat announcement prior to the first walkthrough session (Threat-Threat vs. Safety-Safety and Threat-Safety vs. Safety-Threat) showed poorer recognition memory as compared to the groups that received a safety announcement (P = 0.0468 and P = 0.0426, respectively; Mann-Whitney U test, Cohen's d = 0.5071; effect size r = 0.2458). In conclusion, experimental anxiety induced by the online version of the ToSP leads to compromised recognition memory for complex multi-dimensional information. Our results indicate that cognitive functions of vulnerable populations (with limited mobility) can be evaluated online by means of the ToSP.

Self-focused attention vs. negative attentional bias during public speech task in socially anxious individuals.

Enhanced self-focused attention (SFA) and negative attentional bias (NAB) towards social cues are characteristic hallmarks of social anxiety. It is essential to investigate these two attentional phenomena under socially relevant situations using comparable stimuli. In the present study, individuals with high social anxiety (HSA, n = 32) and low social anxiety (LSA, n = 29) were compared according to their attention toward self-related stimuli and toward positive, neutral, and negative feedback related stimuli. Video stimuli of moving indicators of self-anxiety-status and positive, neutral, and negative feedback from an audience were presented during an impromptu speech task (high anxiety condition) and a re-watching phase (low anxiety condition). Eye movements in response to the different stimuli served as readouts for attentional preference. An interaction effect suggested that the HSA group directed more attention to self-related stimuli relative to other stimuli and the LSA group only during the high anxiety condition. The LSA group exhibited a general attentional preference toward positive feedback, especially during the low anxiety condition. Meanwhile, only the total duration of fixation on positive feedback negatively correlated with subjective anxiety rating. Our results point to increased SFA rather than NAB in HSA individuals under social threats.