Sexual Orientation Affects Neural Responses to Subtle Social Aggression Signals.

The current series of studies are the first to examine brain responses to social aggression signals as a function of male and female sexual orientation. For the first set of studies (1a, 1b), axillary sweat had been collected from 17 heterosexual men and 17 heterosexual women aggressively responding to frustrating opponents (aggression condition) and while playing a construction game (control condition). Sweat samples were pooled according to sex and condition, and presented via a constant flow olfactometer to 17 gay and 23 heterosexual men (Study 1a), and 19 lesbian and 25 heterosexual women (Study 1b). Ongoing EEG was recorded from 61 scalp locations, chemosensory event-related potentials (CSERPs; P2, P3-1, P3-2) were analyzed, and neuronal sources calculated (low resolution electromagnetic tomography). Within the second set of studies (2a, 2b), pictures of males' and females' weak angry and neutral facial expressions were presented to 21 gay and 23 heterosexual men (Study 2a), and 19 lesbian and 26 heterosexual women (Study 2b), and ERPs (N170, P3) were analyzed. Gay men showed larger P3-1 amplitudes than heterosexual men upon presentation of male aggression sweat, accompanied by activation of the right inferior frontal gyrus (IFG, BA 10). Gay men also displayed longer N170 latencies in response to men's compared to women's angry facial expressions, while heterosexual men did not. In women, sexual orientation did not affect the processing of aggression sweat or anger expressions. Gay men showed preferential processing of chemosensory aggression signals (P3-1 amplitudes), indicating fine-tuned socioemotional sensitivity, related to activation of brain areas involved in emotion regulation (IFG). They further process the relative relevance of visual aggression signals (N170 latency). These results were in line with theories proposing a common evolutionary pathway for same-sex attraction and traits easing social integration.

Temporal context modulates sensory attenuation magnitude.

In studies with self-produced sensory events, sensitivity for these events has been found to be reduced. This phenomenon is called sensory attenuation, and it has been assumed that the crucial factor is the self-production of the event. However, this factor may be confounded with the temporal predictability of the event, as well as with attentional focus on the event. In this study, we wondered about the influence of temporal stimulus predictably on sensory attenuation. We asked observers to discriminate the orientation of Gabor patches that were presented randomly at various times around a button press. Despite the unpredictability of stimulus occurrence, attenuation for these stimuli was tuned to the time of the button press. However, temporal expectations determined attenuation magnitude. Sensory attenuation was stronger when stimuli were expected to occur more often before the button press. When stimuli were expected to occur more often after the button press, no sensory attenuation was found. Our results show first that sensory attenuation occurs mandatorily even if stimulus occurrence cannot be predicted temporally. Second, temporal attention, guided by temporal stimulus probabilities, modulates sensory attenuation magnitude.

Chemosensory communication of aggression: women's fine-tuned neural processing of male aggression signals.

The current study is the first to examine the central nervous processing of aggression chemosignals within men and women by means of chemosensory event-related potential (CSERP) analysis. Axillary sweat was collected from 17 men and 17 women participating in a competitive computer game (aggression condition) and playing a construction game (control condition). Sweat samples were pooled with reference to donor gender and condition, and presented to 23 men and 25 women via a constant flow olfactometer. Ongoing electroencephalogram was recorded from 61 scalp locations, CSERPs (P2, P3-1, P3-2) were analysed and neuronal sources calculated (low-resolution electromagnetic tomography, LORETA). Women, especially, showed larger P3-1 and P3-2 amplitudes in response to male as compared with female aggression signals (all p values < 0.01). The peak activation of this effect was related to activity within the dorsomedial prefrontal cortex (Brodmann area 8). As male aggression commonly targets physical harm, the competence of the human brain to sensitively detect male aggression signals is considered to be highly adaptive. The detection of male aggression signals seems to be of higher importance for women than for men. It is suggested that the processing of male aggression signals in women induces an immediate response selection. This article is part of the Theo Murphy meeting issue 'Olfactory communication in humans'.

The effect of space on subjective time is mediated by apparent velocity.

In contrast to the intuitive and traditional assumption of a centralized and universal neural clock, many recent studies have provided evidence against this idea. Here, we investigated whether subjective duration is estimated by a mechanism that tracks the trajectory of a moving object. Such a mechanism would integrate over the velocity and the spatial distance the object traveled to derive its duration. We exposed observers to a moving object that covered either a small or large spatial distance. We found that subjective duration decreased after this exposure when intervals were tested that were defined by stimuli covering a large, but not by stimuli covering a small, spatial distance. We compared the effects of our velocity exposure to previously used adaptation to a drifting grating and found a dependence of spatial distance only for velocity exposure. The finding that temporal estimations decrease after exposure to fast-moving stimuli selectively at large distances suggests that subjective duration is derived from measurements of velocity and space.

The Effect of Cognitive Control on Different Types of Auditory Distraction.

Deviant as well as changing auditory distractors interfere with short-term memory. According to the duplex model of auditory distraction, the deviation effect is caused by a shift of attention while the changing-state effect is due to obligatory order processing. This theory predicts that foreknowledge should reduce the deviation effect, but should have no effect on the changing-state effect. We compared the effect of foreknowledge on the two phenomena directly within the same experiment. In a pilot study, specific foreknowledge was impotent in reducing either the changing-state effect or the deviation effect, but it reduced disruption by sentential speech, suggesting that the effects of foreknowledge on auditory distraction may increase with the complexity of the stimulus material. Given the unexpected nature of this finding, we tested whether the same finding would be obtained in (a) a direct preregistered replication in Germany and (b) an additional replication with translated stimulus materials in Sweden.

Hepatic macrophage migration and differentiation critical for liver fibrosis is mediated by the chemokine receptor C-C motif chemokine receptor 8 in mice.

UNLABELLED: Chemokines critically control the infiltration of immune cells upon liver injury, thereby promoting hepatic inflammation and fibrosis. The chemokine receptor CCR8 can affect trafficking of monocytes/macrophages, monocyte-derived dendritic cells (DCs) and T-helper cell (Th) subsets, but its role in liver diseases is currently unknown. To investigate the functional role of CCR8 in liver diseases, ccr8(-/-) and wild-type (WT) mice were subjected to chronic experimental injury models of carbon tetrachloride (CCl(4) ) administration and surgical bile duct ligation (BDL). CCR8 was strongly up-regulated in the injured liver. Ccr8(-/-) mice displayed attenuated liver damage (e.g., ALT, histology, and TUNEL) compared to WT mice and were also protected from liver fibrosis in two independent injury models. Flow cytometry revealed reduced infiltrates of liver macrophages, neutrophils and natural killer cells, whereas hepatic CD4(+) T cells increased. The main CCR8-expressing cells in the liver were hepatic macrophages, and CCR8 was functionally necessary for CCL1-directed migration of inflammatory but not for nonclassical monocytes into the liver. Moreover, the phenotype of liver macrophages from injured ccr8(-/-) animals was altered with increased expression of DC markers and enhanced expression of T-cell-attracting chemokine macrophage inflammatory protein 1-alpha (MIP-1α/CCL3). Correspondingly, hepatic CD4(+) T cells showed increased Th1 polarization and reduced Th2 cells in CCR8-deficient animals. Liver fibrosis progression, but also subsequent T-cell alterations, could be restored by adoptively transferring CCR8-expressing monocytes/macrophages into ccr8(-/-) mice during experimental injury. CONCLUSIONS: CCR8 critically mediates hepatic macrophage recruitment upon injury, which subsequently shapes the inflammatory response in the injured liver, affecting macrophage/DC and Th differentiation. CCR8 deficiency protects the liver against injury, ameliorating initial inflammatory responses and hepatic fibrogenesis. Inhibition of CCR8 or its ligand, CCL1, might represent a successful therapeutic target to limit liver inflammation and fibrosis progression.