European Journal of Neuroscience最新文献

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.

The continuity illusion occurs when a sound is perceived as continuous through noise-filled interruptions and has been indexed neurophysiologically as reduced auditory theta band (4–8 Hz) power and phase-locking at the interruption boundaries. Here, we examined the behavioural and neurophysiological differences between musicians (n = 16) and nonmusicians (n = 16) as they listened to trisyllabic words and classical music with noise interruptions. Our aim was to assess two competing hypotheses: (H₁) because of their enhanced ability to detect acoustic gaps, musicians are less likely to perceive continuity and will therefore exhibit increased theta power/phase-locking at interruption boundaries compared to nonmusicians. Alternatively, (H₂) musicians are more likely to perceive continuity through an enhanced ability to utilize contextual cues to fill in missing information. This top-down influence should be demonstrated by reduced theta power/phase-locking in musicians. On each trial, participants reported whether a noise-interrupted music or speech stimulus sounded continuous or interrupted. Behaviorally, musicians and nonmusicians had similar rates of perceived continuity for music and speech, except musicians exhibited significantly greater continuity to speech at the shortest noise interruption. The oscillatory results demonstrated that relative to nonmusicians, musicians had weaker theta phase-locking to the interruption boundaries in both music and speech, supporting H₂. Musicians also exhibited enhanced alpha (8–13 Hz) and beta (14–30 Hz) power for both music and speech relative to nonmusicians, possibly reflecting inhibitory processes. We conclude that musicians exhibit enhanced auditory-motor inhibition to noise interruptions in both music and speech and infer this is due to their enhanced ability to utilize contextual cues.

Sleep supports memory formation by neurophysiological mechanisms that are yet to be fully uncovered. We investigated the contribution of the direct coupling of neurons via electrical synapses (gap junctions). The administration of mefloquine (250 mg p.o. vs. placebo), an antimalarial, which blocks electrical synapses, to healthy young men before nocturnal sleep impaired the retention of word pairs learned before drug administration and disrupted the coupling of sleep spindles to EEG slow oscillations. In control experiments, in which participants received mefloquine before a consolidation interval of nocturnal wakefulness or after rather than before sleep, word-pair memory retention was not affected by the drug, suggesting that electrical synapses specifically support the sleep-dependent retention of verbal declarative memory. Irrespective of sleep, mefloquine enhanced the retention of sensorimotor memory assessed with a finger sequence tapping task. In supplemental experiments in rats, mefloquine administered i.p. at escalating doses of 20 and 40 mg/kg did not alter hippocampal sharp-wave/ripple activity, a prominent mechanism of hippocampal memory replay. While mefloquine effects beyond gap junctions in the present experiments cannot be fully excluded, we conclude that electrical coupling enhances the oscillatory coordination between sleep spindles and slow oscillations and, thereby, supports systems memory consolidation.

Synapse elimination during development is crucial for refining neural circuits by removing excess synapses formed around birth. In the neonatal cerebellum, Purkinje cells (PCs) are initially innervated by multiple climbing fibers (CFs) with similar synaptic strengths. During subsequent postnatal development, a single CF is strengthened and retained, while the other CFs are eliminated. Here, our PC-specific RNAi knockdown (KD) screening revealed that fibronectin type III domain containing 3B (FNDC3B), an endoplasmic reticulum protein, was involved in CF synapse elimination from around postnatal day 9 (P9) in mice. We showed that FNDC3B mRNA was expressed in PCs during CF synapse elimination. In PC-selective FNDC3B conditional knockout (FNDC3B-cKO) mice, CF synapse elimination from P10 was impaired, and the extension of CFs along PC dendrites was reduced at P21. However, these phenotypes were recovered by P40. In contrast, parallel fiber-mediated excitatory synaptic inputs and inhibitory synaptic inputs to PCs were not affected in FNDC3B-cKO mice. These results suggest that FNDC3B facilitates CF synapse elimination during postnatal development, highlighting a new role of FNDC3B in the developing brain.