Neuroscience bulletin最新文献

Unlocking task-related EEG spectra is crucial for neuroscience. Traditional convolutional neural networks (CNNs) effectively extract these features but face limitations like overfitting due to small datasets. To address this issue, we propose a lightweight CNN and assess its interpretability through the fully connected layer (FCL). Initially tested with two tasks (Task 1: open vs closed eyes, Task 2: interictal vs ictal stage), the CNN demonstrated enhanced spectral features in the alpha band for Task 1 and the theta band for Task 2, aligning with established neurophysiological characteristics. Subsequent experiments on two brain-computer interface tasks revealed a correlation between delta activity (around 1.55 Hz) and hand movement, with consistent results across pericentral electroencephalogram (EEG) channels. Compared to recent research, our method stands out by delivering task-related spectral features through FCL, resulting in significantly fewer trainable parameters while maintaining comparable interpretability. This indicates its potential suitability for a wider array of EEG decoding scenarios.

The CC chemokine ligand 2 (CCL2, also known as MCP-1) and its cognate receptor CCR2 have well-characterized roles in chemotaxis. CCL2 has been previously shown to promote excitatory synaptic transmission and neuronal excitability. However, the detailed molecular mechanism underlying this process remains largely unclear. In cultured hippocampal neurons, CCL2 application rapidly upregulated surface expression of GluA1, in a CCR2-dependent manner, assayed using SEP-GluA1 live imaging, surface GluA1 antibody staining, and electrophysiology. Using pharmacology and reporter assays, we further showed that CCL2 upregulated surface GluA1 expression primarily via Gα_q- and CaMKII-dependent signaling. Consistently, using i.p. injection of lipopolysaccharide to induce neuroinflammation, we found upregulated phosphorylation of S831 and S845 sites on AMPA receptor subunit GluA1 in the hippocampus, an effect blocked in Ccr2^-/- mice. Together, these results provide a mechanism through which CCL2, and other secreted molecules that signal through G-protein coupled receptors, can directly regulate synaptic transmission.

The activity of occipitotemporal regions involved in linguistic reading processes, such as the ventral occipitotemporal cortex (vOT), is believed to exhibit strong interactions during higher-order language processing, specifically in the connectivity between the occipital gyrus and the temporal gyrus. In this study, we utilized functional magnetic resonance imaging (fMRI) with psychophysiological interaction (PPI) and dynamic causal modeling (DCM) to investigate the functional and effective connectivity in the occipitotemporal network during speed reading. We conducted the experiment with native Japanese speakers who underwent and without speed-reading training and subsequently performed established reading tasks at different speeds (slow, medium, and fast) while undergoing 3-Tesla Siemens fMRI. Our activation analyses revealed significant changes in occipital and temporal regions as reading speed increased, indicating functional connectivity within the occipitotemporal network. DCM results further demonstrated more intricate effective connections and high involvement within the occipitotemporal pathway: (1) reading signals originated from the inferior occipital gyrus (iO), distributed to the vOT and the posterior superior temporal sulcus (pSTS), and then gathered in the anterior superior temporal sulcus (aSTS); (2) reading speed loads had modulation effects on the pathways from the aSTS to vOT and from the iO to vOT. These findings highlight the complex connectivity and dynamic interactions within the occipitotemporal network during speed-reading processes.

Autism Spectrum Disorders (ASDs) are reported as a group of neurodevelopmental disorders. The structural changes of brain regions including the hippocampus were widely reported in autistic patients and mouse models with dysfunction of ASD risk genes, but the underlying mechanisms are not fully understood. Here, we report that deletion of Trio, a high-susceptibility gene of ASDs, causes a postnatal dentate gyrus (DG) hypoplasia with a zigzagged suprapyramidal blade, and the Trio-deficient mice display autism-like behaviors. The impaired morphogenesis of DG is mainly caused by disturbing the postnatal distribution of postmitotic granule cells (GCs), which further results in a migration deficit of neural progenitors. Furthermore, we reveal that Trio plays different roles in various excitatory neural cells by spatial transcriptomic sequencing, especially the role of regulating the migration of postmitotic GCs. In summary, our findings provide evidence of cellular mechanisms that Trio is involved in postnatal DG morphogenesis.

Clinical researches including the Mayo Anesthesia Safety in Kids (MASK) study have found that children undergoing multiple anesthesia may have a higher risk of fine motor control difficulties. However, the underlying mechanisms remain elusive. Here, we report that erythropoietin receptor (EPOR), a microglial receptor associated with phagocytic activity, was significantly downregulated in the medial prefrontal cortex of young mice after multiple sevoflurane anesthesia exposure. Importantly, we found that the inhibited erythropoietin (EPO)/EPOR signaling axis led to microglial polarization, excessive excitatory synaptic pruning, and abnormal fine motor control skills in mice with multiple anesthesia exposure, and those above-mentioned situations were fully reversed by supplementing EPO-derived peptide ARA290 by intraperitoneal injection. Together, the microglial EPOR was identified as a key mediator regulating early synaptic development in this study, which impacted sevoflurane-induced fine motor dysfunction. Moreover, ARA290 might serve as a new treatment against neurotoxicity induced by general anesthesia in clinical practice by targeting the EPO/EPOR signaling pathway.

Autism spectrum disorders (ASD) are characterized by social and repetitive abnormalities. Although the ASD mouse model with Shank3b mutations is widely used in ASD research, the behavioral phenotype of this model has not been fully elucidated. Here, a 3D-motion capture system and linear discriminant analysis were used to comprehensively record and analyze the behavioral patterns of male and female Shank3b mutant mice. It was found that both sexes replicated the core and accompanied symptoms of ASD, with significant sex differences. Further, Shank3b heterozygous knockout mice exhibited distinct autistic behaviors, that were significantly different from those those observed in the wild type and homozygous knockout groups. Our findings provide evidence for the inclusion of both sexes and experimental approaches to efficiently characterize heterozygous transgenic models, which are more clinically relevant in autistic studies.

Fairness is a fundamental value in human societies, with individuals concerned about unfairness both to themselves and to others. Nevertheless, an enduring debate focuses on whether self-unfairness and other-unfairness elicit shared or distinct neuropsychological processes. To address this, we combined a three-person ultimatum game with computational modeling and advanced neuroimaging analysis techniques to unravel the behavioral, cognitive, and neural patterns underlying unfairness to self and others. Our behavioral and computational results reveal a heightened concern among participants for self-unfairness over other-unfairness. Moreover, self-unfairness consistently activates brain regions such as the anterior insula, dorsal anterior cingulate cortex, and dorsolateral prefrontal cortex, spanning various spatial scales that encompass univariate activation, local multivariate patterns, and whole-brain multivariate patterns. These regions are well-established in their association with emotional and cognitive processes relevant to fairness-based decision-making. Conversely, other-unfairness primarily engages the middle occipital gyrus. Collectively, our findings robustly support distinct neurocomputational signatures between self-unfairness and other-unfairness.

The kidneys are essential organs that help maintain homeostasis, and their function is regulated by the neural system. Despite the anatomical multi-synaptic connection between the central autonomic nuclei and the kidneys, it remains unclear whether there are any variations in neural connections between the nervous systems and the renal cortex and medulla in male and female mice. Here, we used the pseudorabies virus to map the central innervation network of the renal cortex and medulla in both sexes. The data revealed that specific brain regions displayed either a contralateral-bias or ipsilateral-bias pattern while kidney-innervating neurons distributed symmetrically in the midbrain and hindbrain. Sex differences were observed in the distribution of neurons connected to the left kidney, as well as those connected to the renal cortex and medulla. Our findings provide a comprehensive understanding of the brain-kidney network in both males and females and may help shed light on gender differences in kidney function and disease susceptibility in humans.

The nervous system is the dominant regulatory system in the human body. The traditional theory is that tumors lack innervation. However, an increasing number of studies have shown complex bidirectional interactions between tumors and the nervous system. Globally, colorectal cancer (CRC) is the third most common cancer. With the rise of tumor neuroscience, the role of nervous system imbalances in the occurrence and development of CRC has attracted increasing amounts of attention. However, there are still many gaps in the research on the interactions and mechanisms involved in the nervous system in CRC. This article systematically reviews emerging research on the bidirectional relationships between the nervous system and CRC, focusing on the following areas: (1) Effects of the nervous system on colon cancer. (2) Effects of CRC on the nervous system. (3) Treatment of CRC associated with the nervous system.