Sören Krach

Anticipation of monetary and social reward differently activates mesolimbic brain structures in men and women

Motivation for goal-directed behaviour largely depends on the expected value of the anticipated reward. The aim of the present study was to examine how different levels of reward value are coded in the brain for two common forms of human reward: money and social approval. To account for gender differences 16 male and 16 female participants performed an incentive delay task expecting to win either money or positive social feedback. fMRI recording during the anticipation phase revealed proportional activation of neural structures constituting the human reward system for increasing levels of reward, independent of incentive type. However, in men activation in the prospect of monetary rewards encompassed a wide network of mesolimbic brain regions compared to only limited activation for social rewards. In contrast, in women, anticipation of either incentive type activated identical brain regions. Our findings represent an important step towards a better understanding of motivated behaviour by taking into account individual differences in reward valuation.

Effects of a CACNA1C genotype on attention networks in healthy individuals.

BACKGROUND Recent genetic studies found the A allele of the variant rs1006737 in the alpha 1C subunit of the L-type voltage-gated calcium channel (CACNA1C) gene to be over-represented in patients with psychosis, including schizophrenia, bipolar disorder and major depressive disorder. In these disorders, attention deficits are among the main cognitive symptoms and have been related to altered neural activity in cerebral attention networks. The particular effect of CACNA1C on neural function, such as attention networks, remains to be elucidated. METHOD The current event-related functional magnetic resonance imaging (fMRI) study investigated the effect of the CACNA1C gene on brain activity in 80 subjects while performing a scanner-adapted version of the Attention Network Test (ANT). Three domains of attention were probed simultaneously: alerting, orienting and executive control of attention. RESULTS Risk allele carriers showed impaired performance in alerting and orienting in addition to reduced neural activity in the right inferior parietal lobule [Brodmann area (BA) 40] during orienting and in the medial frontal gyrus (BA 8) during executive control of attention. These areas belong to networks that have been related to impaired orienting and executive control mechanisms in neuropsychiatric disorders. CONCLUSIONS Our results suggest that CACNA1C plays a role in the development of specific attention deficits in psychiatric disorders by modulation of neural attention networks.

Genetic variation in the schizophrenia-risk gene neuregulin1 correlates with differences in frontal brain activation in a working memory task in healthy individuals

Working memory dysfunctions are a prominent feature in schizophrenia. These impairments have been linked to alterations in prefrontal brain activation with studies reporting hypo- and hyperactivations. Since schizophrenia has a high heritability, it is of interest whether susceptibility genes modulate working memory and its neural correlates. The aim of the present study was to test the influence of the NRG1 schizophrenia susceptibility gene on working memory and its neural correlates in healthy subjects. 429 healthy individuals performed a verbal and a spatial working memory task. A subsample of 85 subjects performed a 2-back version of the Continuous Performance Test (CPT) in a functional MRI study. The NRG1 SNP8NRG221533 (rs35753505) carrier status was determined and correlated with working memory performance and brain activation. There were no effects of genetic status on behavioural performance in the working memory tasks in the 429 subjects and in the fMRI task (n=85). A linear effect of NRG1 SNP8NRG221533 carrier status on neuronal activation emerged in the fMRI experiment. Hyperactivation of the superior frontal gyrus (BA 10) was correlated with the number of risk alleles. The fMRI data suggest that performance measures between groups did not differ due to a compensational activation of BA 10 in risk-allele carriers. Our results are in line with functional imaging studies in patients with schizophrenia, which also showed a differential activation in lateral prefrontal areas.

Understanding social robots: A user study on anthropomorphism

Anthropomorphism is one of the keys to understand the expectations people have about social robots. In this paper we address the question of how a robotpsilas actions are perceived and represented in a human subject interacting with the robot and how this perception is influenced only by the appearance of the robot. We present results of an interaction-study in which participants had to play a version of the classical Prisonerspsila Dilemma Game (PDG) against four opponents: a human partner (HP), an anthropomorphic robot (AR), a functional robot (FR), and a computer (CP). As the responses of each game partner were randomized unknowingly to the participants, the attribution of intention or will to an opponent (i.e. HP, AR, FR or CP) was based purely on differences in the perception of shape and embodiment. We hypothesize that the degree of human-likeness of the game partner will modulate what the people attribute to the opponents - the more human like the robot looks the more people attribute human-like qualities to the robot.

Genetic variation in schizophrenia-risk-gene dysbindin 1 modulates brain activation in anterior cingulate cortex and right temporal gyrus during language production in healthy individuals.

Genetic variation in dysbindin 1 (DTNBP1) gene region tagged by SNP rs1018381 exhibits a linkage with cognitive deficits in patients with schizophrenia and healthy subjects. Language production deficits are core features of schizophrenia with more impairment in semantic than lexical verbal fluency tasks. We investigated the link between brain activation and DTNBP1 SNP rs1018381 during semantic verbal fluency task in a German healthy population. 46 healthy subjects genotyped for SNP rs1018381 status were divided in heterozygous risk-allele carriers (T/C) and homozygous non-carriers (C/C). Neural correlates of semantic verbal fluency were investigated with functional magnetic resonance imaging (fMRI). Stronger right hemispherical brain activation in anterior cingulate gyrus (BA 24), superior (BA 22, 38) and middle (BA 21) temporal gyrus was observed in the carriers compared to non-carriers. Brain activations occurred in the absence of task performance differences. No significant correlations were found between personality traits and brain activation differences. The results point to an influence of genetic variation in DTNBP1 gene region tagged by SNP rs1018381 on neural correlates of language production. Carriers may exhibit higher processing efforts to reach the same behavioural performance as non-carriers as reflected in activation of schizophrenia-related regions.

A putative high risk diplotype of the G72 gene is in healthy individuals associated with better performance in working memory functions and altered brain activity in the medial temporal lobe

G72 is a vulnerability gene for schizophrenia and affective psychosis, disorders that are characterized by deficits in working memory. In the present study we investigated whether the G72 genotype influences verbal and spatial working memory functions in healthy individuals. Working memory was assessed at the behavioural level in 423 subjects using the spatial span of the Wechsler Memory Scale (spatial working memory) and the letter-number-span test (verbal working memory). In a sub-sample of 83 subjects, we assessed working memory functions also at the neural level using functional magnetic resonance imaging during a classical letter variant of the n-back task. Unexpectedly the high risk allele carriers performed better in the verbal working memory task than the other subjects. These behavioural differences were accompanied by brain activation differences in the right parahippocampus, a brain region that plays a major role in schizophrenia and affective disorders. The high risk variant of a vulnerability gene therefore does not necessarily have to negatively affect cognitive abilities per se, but may even have beneficial effects on cognitive functions in the non-affected population.

Affect-specific activation of shared networks for perception and execution of facial expressions

Previous studies have shown overlapping neural activations for observation and execution or imitation of emotional facial expressions. These shared representations have been assumed to provide indirect evidence for a human mirror neuron system, which is suggested to be a prerequisite of action comprehension. We aimed at clarifying whether shared representations in and beyond human mirror areas are specifically activated by affective facial expressions or whether they are activated by facial expressions independent of the emotional meaning. During neuroimaging, participants observed and executed happy and non-emotional facial expressions. Shared representations were revealed for happy facial expressions in the pars opercularis, the precentral gyrus, in the superior temporal gyrus/medial temporal gyrus (MTG), in the pre-supplementary motor area and in the right amygdala. All areas showed less pronounced activation in the non-emotional condition. When directly compared, significant stronger neural responses emerged for happy facial expressions in the pre-supplementary motor area and in the MTG than for non-emotional stimuli. We assume that activation of shared representations depends on the affect and (social) relevance of the facial expression. The pre-supplementary motor area is a core-shared representation-structure supporting observation and execution of affective contagious facial expressions and might have a modulatory role during the preparation of executing happy facial expressions.

Schizophrenie und Schlaf

Neuropsychologie beschaftigt sich uberwiegend mit dem wachen Menschen. Allerdings ist das Gehirn auch im Schlaf aktiv. Deshalb soll hier uber den Zusammenhang zwischen Schlaf und kognitiven Prozessen referiert werden. Alle derzeit vorliegenden Erkenntnisse stutzen einhellig die Hypothese, dass Schlaf nicht mit passiver Regeneration gleichgesetzt werden darf, sondern ein aktiver, zur Wachheit komplementarer Zustand des Gehirns ist. Das naive Modell eines abgeschalteten biologischen Computers wird unserer Nachtruhe in keiner Weise gerecht. Dies trifft auch fur die Energieeinsparung zu, die im Schlaf weitaus geringer ist, als ublicherweise angenommen wird.