NeuroImage
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Events coupled with an emotional context seem to be better retained than non-emotional events. The aim of our study was to investigate whether an emotional context could influence the neural substrates of memory associations with novel portrait art stimuli. In the current prospective fMRI study, we have investigated for one specific visual art form (modern artistic portraits with a high degree of abstraction) whether memory is influenced by priming with emotional facial pictures. ⋯ Importantly, our results also suggest that the negative emotional context leads to the formation of associations that are reactivated during memory retrieval processes of the initially neutral art portraits. When correctly recognized, the portraits evoke neuronal activities consistent with the withdrawal-related character of the emotional visual stimuli with which they have been associated. Although our results show that abstract portrait art can be associated with emotional primes this doesn't mean that this effect is specific for art images.
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Animal and human autopsy studies suggest that subfields of the hippocampal formation are differentially affected by neuropsychiatric diseases. Therefore, subfield volumes may be more sensitive to effects of disease processes. The few human studies that segmented subfields of the hippocampal formation in vivo either assessed the subfields only in the body of the hippocampus, assessed only three subfields, or did not take the differential angulation of the head of the hippocampus into account. ⋯ In conclusion, this study shows that it is possible to delineate the main subfields of the hippocampal formation along its full-length in vivo at 7 T MRI. Our data give evidence that this can be done in a reliable manner. Segmentation of subfields in the full-length of the hippocampus may bolster the study of the etiology neuropsychiatric diseases.
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Social relationships affect empathy in humans such that empathic neural responses to perceived pain were stronger to racial in-group members than to racial out-group members. Why does the racial bias in empathy (RBE) occur and how can we reduce it? We hypothesized that perceiving an other-race person as a symbol of a racial group, rather than as an individual, decreases references to his/her personal situation and weakens empathy for that person. This hypothesis predicts that individuating other-race persons by increasing attention to each individual's feelings or enclosing other-race individuals within one's own social group can reduce the RBE by increasing empathic neural responses to other-race individuals. ⋯ We identified the RBE by showing that, relative to neutral expressions, pain expressions increased neural responses at 128-188 ms after stimulus onset over the frontal/central brain regions, and this effect was evident for same-race faces but not for other-race faces. Experiments 2 and 3 found that paying attention to observed individual's feelings of pain and including other-race individuals in one's own team for competitions respectively eliminated the RBE by increasing neural responses to pain expressions in other-race faces. Our results indicate that the RBE is not inevitable and that manipulations of both cognitive strategies and intergroup relationships can decrease RBE-related brain activity.
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Theta burst stimulation (TBS) is a novel variant of repetitive transcranial magnetic stimulation (rTMS), which induces changes in neuronal excitability persisting up to 1h. When elicited in the primary motor cortex, such physiological modulations might also have an impact on motor behavior. In the present study, we applied TBS in combination with pseudo continuous arterial spin labeling (pCASL) in order to address the question of whether TBS effects are measurable by means of changes in physiological parameters such as cerebral blood flow (CBF) and if TBS-induced plasticity can modify motor behavior. ⋯ It is assumed that inhibitory TBS induced a "local virtual lesion" which leads to the mobilization of more neuronal resources. There was no TBS-specific modulation in motor behavior, which might indicate that acute changes in brain plasticity caused by TBS are immediately compensated. This compensatory reaction seems to be observable at the metabolic, but not at the behavioral level.
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Somatosensory evoked responses are known to be modulated by previous interfering stimuli. Here, we first investigated the modulatory effects of interfering stimuli with different intensities on somatosensory evoked magnetic field in human primary (S1) and secondary (S2) somatosensory cortices. In the control condition of the study, test stimulus, set to strong intensity, was delivered to the left median nerve. ⋯ The extent of amplitude reduction of the bilateral S2 response was markedly increased as intensity of interfering stimuli increased from weak to moderate, but further reduction by the SI stimuli compared to MI stimuli was not observed. Those results indicated that somatosensory cortical activation in the S1 (P35m and P60m) and S2 were modulated by intensity of interfering stimuli. Our findings of a greater gating effect on the bilateral S2 compared to the contralateral S1 indicate that S2 may play an important role in temporal integration of different intensity levels of somatosensory inputs.