Human visual gamma for color stimuli.

Strong gamma-band oscillations in primate early visual cortex can be induced by homogeneous color surfaces (Peter et al., 2019; Shirhatti and Ray, 2018). Compared to other hues, particularly strong gamma oscillations have been reported for red stimuli. However, precortical color processing and the resultant strength of input to V1 have often not been fully controlled for. Therefore, stronger responses to red might be due to differences in V1 input strength. We presented stimuli that had equal luminance and cone contrast levels in a color coordinate system based on responses of the lateral geniculate nucleus, the main input source for area V1. With these stimuli, we recorded magnetoencephalography in 30 human participants. We found gamma oscillations in early visual cortex which, contrary to previous reports, did not differ between red and green stimuli of equal L-M cone contrast. Notably, blue stimuli with contrast exclusively on the S-cone axis induced very weak gamma responses, as well as smaller event-related fields and poorer change-detection performance. The strength of human color gamma responses for stimuli on the L-M axis could be well explained by L-M cone contrast and did not show a clear red bias when L-M cone contrast was properly equalized.

Stimulus-specific plasticity in human visual gamma-band activity and functional connectivity.

Under natural conditions, the visual system often sees a given input repeatedly. This provides an opportunity to optimize processing of the repeated stimuli. Stimulus repetition has been shown to strongly modulate neuronal-gamma band synchronization, yet crucial questions remained open. Here we used magnetoencephalography in 30 human subjects and find that gamma decreases across ≈10 repetitions and then increases across further repetitions, revealing plastic changes of the activated neuronal circuits. Crucially, increases induced by one stimulus did not affect responses to other stimuli, demonstrating stimulus specificity. Changes partially persisted when the inducing stimulus was repeated after 25 minutes of intervening stimuli. They were strongest in early visual cortex and increased interareal feedforward influences. Our results suggest that early visual cortex gamma synchronization enables adaptive neuronal processing of recurring stimuli. These and previously reported changes might be due to an interaction of oscillatory dynamics with established synaptic plasticity mechanisms.

Probing the causal involvement of dlPFC in directed forgetting using rTMS-A replication study.

The forgetting of previously remembered information has, for a long time, been explained by purely passive processes. This viewpoint has been challenged by the finding that humans show worse memory for specific items that they have been instructed to forget. The dorsolateral prefrontal cortex has, through imaging, lesion and brain stimulation studies, been implied in controlling such active forgetting processes. In this study, we attempted to solidify evidence for such a causal role of the dlPFC in directed forgetting by replicating an existing rTMS study (Hanslmayr S, 2012) in a preregistered within-participant design. We stimulated participants at the dlPFC (BA9) or vertex using 45s of 1Hz rTMS after instructions to forget previously remembered words in a list-method directed forgetting paradigm and tested for effects on the amount of forgotten information. Contrary to the study we were attempting to replicate, no significant increase in forgetting under dlPFC stimulation was found in our participants. However, when combining our results with the study we were attempting to replicate, dlPFC stimulation led to significantly increased directed forgetting in both studies combined. We further explored if the rTMS parameters used here and in earlier work (Hanslmayr S, 2012) influenced inhibitory processing at their time of delivery or in a more persistent manner. Unaltered incongruency and negative priming effects in a Stroop task conducted directly after stimulation suggests that our rTMS stimulation did not continue to influence inhibitory processing after the time of stimulation. As the combined evidence for increased directed forgetting due to rTMS dlPFC stimulation is still quite weak, additional replications are necessary to show that directed forgetting is indeed causally driven by an active prefrontal process.

Glucocorticoid receptor gene methylation moderates the association of childhood trauma and cortisol stress reactivity.

Exposure to childhood trauma (CT) has been linked to sustained dysregulations of major stress response systems, including findings of both exaggerated and attenuated hypothalamus-pituitary-adrenal (HPA) axis activity. Likewise, CT constitutes a common risk factor for a broad range of psychiatric conditions that involve distinct neuroendocrine profiles. In this study, we investigated the role of epigenetic variability in a stress-related gene as a potential mediator or moderator of such differential trajectories in CT survivors. For this, we screened adult volunteers for CT and recruited a healthy sample of 98 exposed (67 with mild-moderate, 31 with moderate-severe exposure) and 102 control individuals, with an equal number of males and females in each group. DNA methylation (DNAM) levels of the glucocorticoid receptor exon 1F promoter (NR3C1-1F) at functionally relevant sites were analyzed via bisulfite pyrosequencing from whole blood samples. Participants were exposed to a laboratory stressor (Trier Social Stress Test) to assess salivary cortisol stress responses. The major finding of this study indicates that DNAM in a biologically relevant region of NR3C1-1F moderates the specific direction of HPA-axis dysregulation (hypo- vs. hyperreactivity) in adults exposed to moderate-severe CT. Those trauma survivors with increased NR3C1-1F DNAM displayed, on average, 10.4 nmol/l (62.3%) higher peak cortisol levels in response to the TSST compared to those with low DNAM. In contrast, unexposed and mildly-moderately exposed individuals displayed moderately sized cortisol stress responses irrespective of NR3C1-1F DNAM. Contrary to some prior work, however, our data provides no evidence for a direct association of CT and NR3C1-1F DNAM status. According to this study, epigenetic changes of NR3C1-1F may provide a more in-depth understanding of the highly variable neuroendocrine and pathological sequelae of CT.