European Journal of Neuroscience最新文献

After concurrent visual and tactile stimuli have been presented repeatedly with a spatial offset, unisensory tactile stimuli, too, are perceived with a spatial bias towards the previously presented visual stimuli. This so-called visual-tactile ventriloquism aftereffect reflects crossmodal recalibration. As touch is intrinsically linked to body parts, we asked here whether recalibration occurs at the level of individual stimuli or at a higher, integrated, map-like level. We applied tactile stimuli to participants' hidden left hand and simultaneously presented visual stimuli with spatial offsets that, if integrated with the tactile stimuli, implied a larger hand. After recalibration, participants pointed to tactile-only stimuli and judged the distance between two tactile stimuli on the hand. The pattern of changes in tactile localization after recalibration was consistent with participants aiming at targets on an enlarged hand. This effect was evident also for new, tactile-only locations that had not been paired with visual stimuli during recalibration. In contrast, distance judgements were not consistently affected by recalibration. The generalization of recalibration to new, non-trained stimulus sites, but not across tasks and responses, suggests a link of low-level multisensory processing and map-like body representations that may, however, be purpose-specific and not organized as a general-purpose "body schema".

Sickness sleep and rebound following sleep deprivation share humoral signals including the rise of cytokines, in particular interleukins. Nevertheless, they represent unique physiological states with unique brain firing patterns and involvement of specific circuitry. Here, we performed untargeted metabolomics of mouse cortex and hippocampus to uncover changes with sickness and rebound sleep as compared with normal daily sleep. We found that the three settings are biochemically unique with larger differences in the cortex than in the hippocampus. Both sickness and rebound sleep shared an increase in tryptophan. Surprisingly, these two sleep conditions showed opposite modulation of the methionine-homocysteine cycle and differences in terms of the energetic signature, with sickness impinging on glycolysis intermediates whilst rebound increased the triphosphorylated form of nucleotides. These findings indicate that rebound following sleep deprivation stimulates an energy rich setting in the brain that is devoid during sickness sleep.

Spinal cord injury (SCI) is a devastating injury that significantly impairs patients' quality of life. To date, there is no effective treatment to mitigate nerve tissue damage and restore neurological function. Neural stem cells (NSCs) derived from human embryonic stem cells (hESCs) are considered an important cell source for reconstructing damaged neural circuits and enabling axonal regeneration. Recent preclinical studies have shown that NSCs are potential therapeutic cell sources for neuroprotection and neuroregeneration in SCI animal models. NSCs can be derived from different sources and the spinal cord-specific NSCs have a higher potential for the regeneration of SCI. However, the long-term therapeutic efficacy of spinal cord-specific NSCs remains unproven. Here, we generated human spinal cord NSCs (hSCNSCs) and investigated the effects of transplanted hSCNSCs on the repair of the SCI model rats for 60 days. The transplanted hSCNSCs improved BBB scores, reduced the lesion area and promoted an increase in the number of Nestin-positive cells in the spinal cord compared to the model rats. Meanwhile, hSCNSC transplantation promoted the expression of synaptophysin, a synaptic signature protein and MBP, a protein associated with remyelination. Interestingly, BAF45D, a chromatin remodelling factor that contributes to the induction of hSCNSCs with region-specific spinal cord identity, were increased by the hSCNSC transplantation. In addition, conditioned medium derived from the hSCNSCs also promoted regenerative repair of the injured spinal cord. These results demonstrate that hSCNSCs may play a critical role in the regenerative repair of SCI.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the presence of β-amyloid (Aβ)-containing extracellular neuritic plaques and phosphorylated tau-containing intracellular neurofibrillary tangles. It remains the primary neuropathological criteria for the diagnosis of AD. Additionally, several other processes are currently being recognized as significant risk factors for AD development, including the brain's susceptibility to reactive oxygen species (ROS). The ROS production is among the early signs in the progression of AD. However, the underlying mechanisms behind increased ROS production in AD remain poorly understood. We have observed SNTA1 plays critical role in regulating ROS levels in different pathological conditions. Here, we wanted to gain further insight into the role of SNTA1 in the development of AD by using IMR32 cell line. Our results show that the accumulation of Aβ plaques in Alzheimer's model neuroblastoma cells significantly increases the expression and activation of SNTA1 and MKK6 kinase. The activation of MKK6 results in the phosphorylation of SNTA1, creating a binding site for Rac1, leading to its activation and subsequent production of ROS. Excessive ROS production leads to cell cycle arrest in the G2/M phase, a hallmark of AD. Our study provides new insight into the mechanism of Aβ-mediated cell death in AD and suggests that MKK6-mediated activation of alpha-1-syntrophin promotes ROS production in neuronal cells, resulting in cell death. This study presents a mechanistic insight into Aβ-mediated cell death and could serve as a paradigm for reducing neuronal cell death in AD.

In this latest addition to the Profiles of Women in Neuroscience series by EJN, Dr. Laurel Trainor discusses her unique academic journey and current research. She describes how she blends being a musician and a neuroscientist to ask riveting questions about the human brain's love for rhythm and communication. This conversation with Trainor also gives insights on succeeding in the field, protecting time for work-life balance and where neuroscience research may be heading in the future.

There has been a lot of controversy regarding mirror neuron function in autism spectrum disorder (ASD), in particular during the observation of biological motions (BM). Here, we directly explored the link between visual attention and brain activity in terms of mu suppression, by simultaneously recording eye-tracking and EEGs during BM tasks. Nineteen autistic children (15 boys, mean age = 11.57 ± 4.28 years) and 19 age-matched neurotypical (NT) children (15 boys, mean age = 11.68 ± 5.22 years) participated in the study. Each participant's eye movement and EEG were simultaneously recorded while watching four BM stimuli (walking, cartwheeling, free-throwing and underarm throwing) and a scrambled condition. Mu (8-13 Hz) suppression index (SI) for central regions was calculated. Fixation counts and percent of fixation time were calculated as indices of eye movements. EEG results revealed significant mu suppressions in the central region in both groups for all BM actions. Eye-tracking results showed that NT children had greater fixation counts and a higher percentage of fixation time than autistic children, indicating greater overall visual attention to BM. Notably, correlational analyses for both groups further revealed that individuals' fixation time and fixation counts were negatively correlated with the mu suppression index for all actions, indicating a strong association between visual attention and mu SI in the central region. Our findings suggest a critical role of visual attention in interpreting mu suppression during action perception in autism.

The brain's ability to integrate sensory and motor information allows us to maintain a sense of orientation in space, a process in which head-direction cells play a key role. While these neurons have been studied extensively in mammals, their presence and function in non-mammalian species remain less understood. Here, I summarize the research work for my PhD thesis, where we explore the interpeduncular nucleus (IPN) in zebrafish, a lesser known brain region, using whole-brain electron microscopy and calcium imaging techniques. We identified a novel population of unipolar neurons, with their activity exhibiting a dynamic, rotational pattern during head movements, even in the absence of sensory cues. This population mirrors the functionality of head-direction cells observed in mammals, suggesting a conserved mechanism for spatial orientation across vertebrates. Our findings reveal the potential of the zebrafish IPN as a vertebrate model for studying ring attractor networks, a theoretical framework previously used to explain head-direction cell activity. These results pave the way for future research on how motor and sensory signals converge in the vertebrate brain to maintain spatial orientation.

Alzheimer's disease (AD) is the most common neurodegenerative disease, and it is currently untreatable. RNA sequencing (RNA-Seq) is commonly used in the literature to identify AD-associated molecular mechanisms by analysing changes in gene expression. RNA-Seq data can also be used to detect genomic variants, enabling the identification of the genes with a higher load of deleterious variants in patients compared with controls. Here, we analysed AD RNA-Seq datasets to obtain differentially expressed genes and genes with a higher load of pathogenic variants in AD, and we combined them in a single list. We mapped these genes on a human protein-protein interaction network to discover subnetworks perturbed by AD. Our results show that utilizing gene pathogenicity information from RNA-Seq data positively contributes to the disclosure of AD-related mechanisms. Moreover, dividing the discovered subnetworks into highly connected modules reveals a clearer picture of altered molecular pathways that, otherwise, would not be captured. Repeating the whole pipeline with human metabolic network genes led to results confirming the positive contribution of gene pathogenicity information and enabled a more detailed identification of altered metabolic pathways in AD.

RETRACTION: Q. He, Y. Li, S. Guo, Y. Wang, W. Lin, Q. Zhang, J. Wang, C. Ma, and B. Xiao, “Inhibition of Rho-kinase by Fasudil Protects Dopamine Neurons and Attenuates Inflammatory Response in an Intranasal Lipopolysaccharide-Mediated Parkinson's Model,” European Journal of Neuroscience 43, no. 1 (2016): 41–52, https://doi.org/10.1111/ejn.13132

The above article, published online on 13 November 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editors-in-Chief, John Foxe and Yoland Smith; the Federation of European Neuroscience Societies; and John Wiley & Sons Ltd. The retraction has been agreed due to concerns raised by another publisher that portions of Figure 6 were duplicated from an earlier publication by this research group. An internal investigation by Wiley confirmed the image duplications in this figure. The authors acknowledged this mistake but were unable to provide a satisfactory explanation to address the concerns. The retraction has been agreed because of the effect of this duplication on the interpretation of the data and results presented.