European Journal of Neuroscience最新文献

To interact efficiently with our environment, our brain predicts the sensory effects of our actions and compares them with the actual outcomes. This allows us to adapt our actions when predictions and sensory outcomes mismatch. While this process is generally well understood for action-sound predictions, it is an open question whether these predictions can flexibly switch in frequently changing environments, as they occur in real life. To investigate the flexibility of top-down predictions, we asked participants (N = 41) to press one of two buttons, a left-hand and a right-hand button, and switch hands autonomously. One button frequently produced a sound (80%) and rarely no sound. The other button frequently generated no sound (80%) and rarely produced a sound. In a third, separate condition, each button produced a sound in 50% of the trials. Unexpected sounds and unexpected sound omissions elicited a series of error-related brain responses in the electroencephalogram (EEG) at different levels of auditory processing, including a mismatch negativity (MMN) and the P3 complex for unexpected sounds, and the oN1, oN2, and oP3 complex for unexpected omissions. Moreover, unexpected sounds elicited an equivalent MMN, regardless of whether silence was expected (80%) or no reliable expectation was possible (50%), while later P3 components showed different amplitudes. Our results demonstrate flexible action-sound predictions at sensory and higher cortical levels. Furthermore, they indicate that predicted silence does not have an explicit sensory representation at lower levels but emerges at later stages, when higher-level information has been integrated.

Caffeine, the most used global stimulant, can impact neurocognition. Hormonal fluctuations occurring across the human menstrual cycle affect similar cognitive domains. Research is needed to identify whether the purported cognitive-enhancing effects of caffeine vary across menstrual cycle phase. The objective of this study was to examine the impact of caffeine on EEG-derived markers of auditory change detection and novelty processing (MMN, P3a, P3b and RON) across phases of the menstrual cycle in naturally cycling females. Participants were randomly assigned to complete the experiment while in their menstrual (n = 31), follicular (n = 26) or luteal (n = 29) phase, completing two sessions wherein they were administered either a caffeine pill (200 mg, oral) or a placebo in a counterbalanced order using a randomized, double-blinded procedure. Auditory tone detection was assessed via a novelty oddball task while EEG data were collected. Caffeine significantly enhanced target detection at both the neural (P3b, MMN and RON) and behavioural levels, with effects most prominent in the menstrual phase. Additionally, P3a and P3b amplitudes differed significantly between phase groups under placebo conditions but not under caffeine conditions. Caffeine significantly enhanced target detection at both the electrophysiological and behavioural levels, with these effects mostly limited to the menstrual phase. Additionally, there were significant differences in ERP activity between all menstrual phases under both placebo and caffeine conditions. Our results suggest that caffeine enhances auditory novelty processing, particularly during the menstrual phase, though future research is needed to further explore the intersection of caffeine and the HMC.

The relationship between primary (S1) and secondary (S2) somatosensory cortex is not well understood, and the role of S2 in somatosensory function is not well defined. To test the role of S2 and its interplay with S1 in learning a texture discrimination, we reversibly inhibited primary (S1) and/or secondary somatosensory cortex (S2) bilaterally using DREADDs and measured the effect on the ability of mice to learn a whisker-dependent tactile discrimination. Freely moving mice foraged in an arena that contained two bowls, one of which contained a buried food reward. The bowls could only be distinguished by the texture on the outer surface. DREADD-mediated inhibition suppressed sensory responses and disrupted network activity in the cortical area in which DREADDs were expressed. We found that both S1 and S2 were critical for learning the tactile discrimination. Tactile learning in naive mice required normal S2 function during the learning phase but not during the post-training consolidation phase of approximately 6 h. Furthermore, S2 was only required during learning. Once expert levels of discrimination had been attained, S2 was not required for execution of the learned discrimination. The role of S2 was confined to tactile learning and was not required for olfactory discrimination. Our findings suggest that S1 and S2 interact when learning a new tactile discrimination, but the learned skill eventually becomes independent of S2.

Tsetse flies (Glossina sp.) are important disease vectors with unique biology that makes them fascinating models to study the evolution of behaviour and its underlying neural circuits. They evolved blood-feeding in an independent event from mosquitoes, and unlike most insects, give birth to a single live offspring—rather than laying eggs. Given their impact on public health, they have been extensively studied with a strong focus on vector control. However, information on their sensory ecology and neurobiology is thinly spread across the literature. Here, we review over a hundred years of literature on tsetse sensory systems, including olfaction, vision, audition, taste, thermosensation and mechanosensation, in the context of the behaviours they drive, including host-finding, blood-feeding and mating. We embed the available data within our more detailed understanding of the sensory systems of the vinegar fly Drosophila melanogaster and other diptera. This sets the stage for future work on how tsetse find their hosts and reproduce, opening new avenues to understand how their sensory systems function and evolve, which in turn will inform better control strategies to reduce the burden of the diseases they transmit.

Uncertainty is a key contributor to decision making, and humans show inconsistent attitudes towards it. Although excessive uncertainty-avoidance or uncertainty-seeking are hallmark symptoms of several mental conditions, the neural mechanism underlying uncertainty seeking and avoidance remains unclear. Here, we probed whether changes in pupil-linked arousal are indicative of uncertainty avoidance in humans. Investigating baseline pupil size to capture endogenous fluctuations across two experiments (N₁ = 24, N₂ = 21), we found that pretrial pupillary responses (as early as 700 ms prior to the onset of a trial) were closely related to uncertainty attitudes during multiarmed bandit tasks. Although increased baseline pupil size signalled avoidance in uncertainty-related decisions, it did not foreshadow value processing per se. The specificity of our results suggests that uncertainty processing is dynamic and depends on (potentially noradrenergic) endogenous pupil fluctuations.

Zhang, Y-Y, Song, N, Liu, F, et al. 2020. Activation of the RAS/B-RAF-MEK-ERK Pathway in Satellite Glial Cells Contributes to Substance p-Mediated Orofacial Pain. European Journal of Neuroscience 51: 2205–2218. https://doi.org/10.1111/ejn.14619.

The fluorescence image of the Veh group for PKC in Figure 4a was inadvertently misused during the figure preparation process. To rectify this issue, we have prepared a revised version of Figure 4 with the corrected image below.

We apologize for this error.

Freezing of gait (FOG) is a disabling feature of Parkinson's Disease (PD) with unclear underlying pathophysiology. Evidence from multimodal neuroimaging studies suggests that complex interactions between cortical and subcortical areas may occur in FOG. While noninvasive neuromodulation techniques, such as transcranial magnetic stimulation (TMS), can effectively modulate large-scale networks involved in FOG, the development of noninvasive neuromodulation interventions is limited by an incomplete understanding of the interactions between underlying network disruptions and FOG behavior. Recent studies have brought into question whether observed network changes in FOG are truly causal or secondary, and if secondary, are they adaptive, maladaptive, or not related? Although these questions go beyond correlative analyses, neuromodulation approaches provide an opportunity to systematically alter networks involved in FOG, providing evidence of a causal relationship. Here, we present evidence from noninvasive neuromodulation interventions of multiple cortical targets and their effects on behavior. In an attempt to leverage prior work to shed light onto the pathophysiology of FOG, we provide specific definitions of key aspects of gait behavior. We also aim to provide a framework under which adaptive and maladaptive network changes can be interpreted and targeted for the development of neuromodulation interventions. We encourage the design of future neuromodulation studies to consider including multimodal outcomes that will expand our understanding of the relationship between FOG behavior and treatment related network changes.