Frontiers in Neuroscience

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ISSN / EISSN : 1662-453X / 1662-453X
Current Publisher: Frontiers Media SA (10.3389)
Total articles ≅ 10,019
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Xue-Hui Zhang, Chen-Chen Feng, Li-Jian Pei, Ya-Nan Zhang, Liu Chen, Xu-Qiang Wei, Jia Zhou, Yue Yong,
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.657507

Abstract:
Neuropathic pain (NeuP) is an important clinical problem accompanying negative mood symptoms. Neuroinflammation in the amygdala is critically involved in NeuP, and the dopamine (DA) system acts as an important endogenous anti-inflammatory pathway. Electroacupuncture (EA) can improve the clinical outcomes in NeuP, but the underlying mechanisms have not been fully elucidated. This study was designed to assess the effectiveness of EA on pain and pain-related depressive-like and anxiety-like behaviors and explore the role of the DA system in the effects of EA. Male Sprague-Dawley rats were subjected to the chronic constrictive injury (CCI) model to induce NeuP. EA treatment was carried out for 30 min once every other day for 3 weeks. The results showed that CCI caused mechanical hyperalgesia and depressive and anxiety-like behaviors in rats and neuroinflammation in the amygdala, such as an increased protein level of TNFα and IL-1β and activation of astrocytes. EA treatment significantly improved mechanical allodynia and the emotional dysfunction induced by CCI. The effects of EA were accompanied by markedly decreased expression of TNFα, IL-1β, and glial fibrillary acid protein (GFAP) in the amygdala. Moreover, EA treatment reversed CCI-induced down-regulation of DA concentration, tyrosine hydroxylase (TH) expression, and DRD1 and DRD2 receptors. These results suggest that EA-ameliorated NeuP may possibly be associated with the DA system to inhibit the neuroinflammation in the amygdala.
Olayinka Oladosu, Wei-Qiao Liu, Bruce G. Pike, Marcus Koch, Luanne M. Metz, Yunyan Zhang
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.634063

Abstract:
Tissue pathology in multiple sclerosis (MS) is highly complex, requiring multi-dimensional analysis. In this study, our goal was to test the feasibility of obtaining high angular resolution diffusion imaging (HARDI) metrics through single-shell modeling of diffusion tensor imaging (DTI) data, and investigate how advanced measures from single-shell HARDI and DTI tractography perform relative to classical DTI metrics in assessing MS pathology. We examined 52 relapsing-remitting MS patients who had 3T anatomical brain MRI and DTI. Single-shell HARDI modeling yielded 5 sub-voxel-based metrics, totalling 11 diffusion measures including 4 DTI and 2 tractography metrics. Based on machine learning of 3-dimensional regions of interest, we evaluated the importance of the measures through several tissue classification tasks. These included two within-subject comparisons: lesion versus normal appearing white matter (NAWM); and lesion core versus shell. Further, by stratifying patients as having high (above 75% ile ) and low (below 25% ile ) number of MS lesions, we also performed 2 classifications between subjects for lesions and NAWM respectively. Results showed that in lesion-NAWM analysis, HARDI orientation distribution function (ODF) energy, DTI fractional anisotropy (FA), and HARDI orientation dispersion index were the top three metrics, which together achieved 65.2% accuracy and 0.71 area under the receiver operating characteristic curve (AUROC). In core-shell analysis, DTI mean diffusivity (MD), radial diffusivity, and FA were the top three metrics, and MD dominated the classification, which achieved 59.3% accuracy and 0.59 AUROC alone. Between patients, FA was the leading feature in lesion comparisons, while ODF energy was the best in NAWM separation. Collectively, single-shell modeling of common diffusion data can provide robust orientation measures of lesion and NAWM pathology, and DTI metrics are most sensitive to intra-lesion abnormality. Combined analysis of both advanced and classical diffusion measures may be critical for improved understanding of MS pathology.
Adam R. Stinchcombe, Caiping Hu, Olivia J. Walch, Samuel D. Faught, Kwoon Y. Wong,
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.652996

Abstract:
Proper circadian photoentrainment is crucial for the survival of many organisms. In mammals, intrinsically photosensitive retinal ganglion cells (ipRGCs) can use the photopigment melanopsin to sense light independently from rod and cone photoreceptors and send this information to many brain nuclei such as the suprachiasmatic nucleus (SCN), the site of the central circadian pacemaker. Here, we measure ionic currents and develop mathematical models of the electrical activity of two types of ipRGCs: M1, which projects to the SCN, and M4, which does not. We illustrate how their ionic properties differ, mainly how ionic currents generate lower spike rates and depolarization block in M1 ipRGCs. Both M1 and M4 cells have large geometries and project to higher visual centers of the brain via the optic nerve. Using a partial differential equation model, we show how axons of M1 and M4 cells faithfully convey information from the soma to the synapse even when the signal at the soma is attenuated due to depolarization block. Finally, we consider an ionic model of circadian photoentrainment from ipRGCs synapsing on SCN neurons and show how the properties of M1 ipRGCs are tuned to create accurate transmission of visual signals from the retina to the central pacemaker, whereas M4 ipRGCs would not evoke nearly as efficient a postsynaptic response. This work shows how ipRGCs and SCN neurons' electrical activities are tuned to allow for accurate circadian photoentrainment.
Sentiljana Gumeni, Chiara Vantaggiato, Monica Montopoli,
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.660714

Abstract:
Hereditary spastic paraplegia (HSP) is a group of inherited neurodegenerative conditions that share a characteristic feature of degeneration of the longest axons within the corticospinal tract, which leads to progressive spasticity and weakness of the lower limbs. Mutations of over 70 genes produce defects in various biological pathways: axonal transport, lipid metabolism, endoplasmic reticulum (ER) shaping, mitochondrial function, and endosomal trafficking. HSPs suffer from an adequate therapeutic plan. Currently the treatments foreseen for patients affected by this pathology are physiotherapy, to maintain the outgoing tone, and muscle relaxant therapies for spasticity. Very few clinical studies have been conducted, and it’s urgent to implement preclinical animal studies devoted to pharmacological test and screening, to expand the rose of compounds potentially attractive for clinical trials. Small animal models, such as Drosophila melanogaster and zebrafish, have been generated, analyzed, and used as preclinical model for screening of compounds and their effects. In this work, we briefly described the role of HSP-linked proteins in the organization of ER endomembrane system and in the regulation of ER homeostasis and stress as a common pathological mechanism for these HSP forms. We then focused our attention on the pharmacodynamic and pharmacokinetic features of some recently identified molecules with antioxidant property, such as salubrinal, guanabenz, N-acetyl cysteine, methylene blue, rapamycin, and naringenin, and on their potential use in future clinical studies. Expanding the models and the pharmacological screening for HSP disease is necessary to give an opportunity to patients and clinicians to test new molecules.
Zihu Tan, Jing Qiu, Yuting Zhang, Qiong Yang, Xixi Yin, Jia Li, Guangya Liu, Hengfei Li, Guang Yang
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.646537

Abstract:
Behavioral and psychological symptoms of dementia (BPSD) ubiquitously disturb all patients with dementia at some point in the disease course. Although a plethora of non-pharmacological and pharmacological methods targeting the relief BPSD have been developed, the therapeutic effect is still far from ideal. Here, a rat BPSD model combining the physiological changes with mental insults was successfully established. Meanwhile, our results indicated that TMP attenuated anxious behavior using an elevated plus maze (EPM) test, ameliorated recognitive ability and sociability through a novel object recognition test (NORT) and social interaction test (SIT), and improved learning and memory impairments via a Barnes maze in rats with bilateral common carotid arteries occlusion (BCCAO) plus chronic restraint stress (CRS). Given that hippocampus chronic cerebral hypoperfusion (CCH) always causes damage to the hippocampus, and the majority of cognitive impairments, behaviors, and stress responses are associated with pathology in the hippocampus including anxiety and depression, we paid attention to investigate the role of the hippocampus in BPSD. Our results indicated that Tetramethylpyrazine (TMP) attenuated anxiety and ameliorated recognitive ability, sociability, learning, and memory impairments due to alleviating dendritic and spine deficits, and upregulating the expression of synapse-related proteins (including PSD95, SYN, GAP43, SYP) in the hippocampus. We also found that the underlying mechanism was that TMP could activate the TrkB/ERK/CREB signaling pathway to promote synaptic remodeling in vivo and in vitro. Mechanically, the present study enlarges the therapeutic scope of TMP in neurodegenerative disorders and provides basic knowledge and feasible candidates for treating BPSD, particularly for vascular dementia.
Yi Gu, Lei Hua
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.685119

Abstract:
The brain is the central nervous system that governs human activities. However, in modern society, more and more diseases threaten the health of the brain and nerves and spinal cord, making the human brain unable to conduct normal information interaction with the outside world. The rehabilitation training of the brain-computer interface can promote the nerve repair of the sensorimotor cortex in patients with brain diseases. Therefore, the research of brain-computer interface for motor imaging is of great significance for patients with brain diseases to restore motor function. Due to the characteristics of non-stationary, nonlinear, and individual differences of EEG signals, there are still many difficulties in the analysis and classification of EEG signals at this stage. In this study, the Extreme Learning Machine (ELM) model was used to classify motor-imaging EEG signals, identify the user’s intention, and control external devices. Considering that single-modal features cannot represent the core information, this study uses a fusion feature that combines temporal and spatial features as the final feature data. The fusion features are input to the trained ELM classifier, and the final classification result is obtained. Two sets of BCI competition data in the BCI competition public database are used to verify the validity of the model. The experimental results show that the ELM model has achieved a classification accuracy of 0.7832 in the classification task of Data Sets IIb, which is higher than other comparison algorithms, and shows universal applicability among different subjects. In addition, the average recognition rate of this model in the Data Sets IIIa classification task reaches 0.8347, which has obvious advantages compared with the comparative classification algorithm. The classification effect is smaller than the classification effect obtained by the champion algorithm of the same project, which has certain reference value.
Yi Lv, Haijun Luo
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.659095

Abstract:
Hemorrhage imaging is one of the most common applications of magnetic induction tomography (MIT). Depth and the mass of stroke stimulated (MSS) are the most important issues that need to be solved for this application. Transcranial magnetic stimulation (TMS) is a technique belonging to the deep brain stimulation (DBS) field, which aims at overcoming human diseases such as depression. TMS coils, namely, circular, figure-8, and H-coils, play an important role in TMS. Among these, H-coils individually focus on the issues of achieving effective stimulation of deep region. MIT and TMS mechanisms are similar. Herein, for the first time, improved TMS coils, including figure-8 and H-coils, are applied as MIT excitation coils to study the possibility of achieving the mass of stroke stimulated and deep detection through MIT. In addition, the configurations of the detection coils are varied to analyze their influence and determine the optimal coils array. Finally, MIT is used to detect haemorrhagic stroke occurring in humans, and the application of deep MIT to the haemorrhagic stroke problem is computationally explored. Results show that among the various coils, the improved H-coils have MSS and depth characteristics that enable the detection of deep strokes through MIT. Although the detecting depth of the figure-8 coil is weaker, its surface signal is good. The deep MIT technique can be applied to haemorrhagic detection, providing a critical base for deeper research.
, Christoph Mulert
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.643597

Abstract:
Visual attention is the cognitive process that mediates the selection of important information from the environment. This selection is usually controlled by bottom-up and top-down attentional biasing. Since for most humans vision is the dominant sense, visual attention is critically important for higher-order cognitive functions and related deficits are a core symptom of many neuropsychiatric and neurological disorders. Here, we summarize the importance and relative contributions of different neuromodulators and neurotransmitters to the neural mechanisms of top-down and bottom-up attentional control. We will not only review the roles of widely accepted neuromodulators, such as acetylcholine, dopamine and noradrenaline, but also the contributions of other modulatory substances. In doing so, we hope to shed some light on the current understanding of the role of neurochemistry in shaping neuron properties contributing to the allocation of attention in the visual field.
Corrigendum
Fengyun Yu, Xinwei Tang, Ruiping Hu, Sijie Liang, Weining Wang, Shan Tian, Yi Wu, Ti-Fei Yuan, Yulian Zhu
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.687972

Abstract:
A Corrigendum on The After-Effect of Accelerated Intermittent Theta Burst Stimulation at Different Session Intervals by Yu, F., Tang, X., Hu, R., Liang, S., Wang, W., Tian, S., et al. (2020). Front. Neurosci. 14:576. doi: 10.3389/fnins.2020.00576 In the original article, there was a mistake in the legend for Figure 5(C) and Figure 6(D) as published. It should be “iTBS600×3*30,” but it was written incorrectly to “iTBS×3*10.” The correct legend appears below. Figure 5. Individual response to iTBS after 1800 pulses stimulation in three different intervals. (A) iTBS1800 (B) iTBS600 × 3*10 (C) iTBS600 × 3*30. Figure 6. The percentage of subjects that responded to different iTBS conditions. (A) one blocks of iTBS (B) iTBS1800 (C) iTBS600 × 3*10 (D) iTBS600 × 3*30. In the original article, there was a mistake in Table 2 as published. The corrected Table 2 appears below. The SI1mv data for iTBS600×3*10 was incorrectly filled in as 198.2. Table 2. Subjects' baseline RMT, MEP amplitude, SI1mv, and LICI when started three different iTBS conditions. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated. Keywords: theta burst stimulation, accelerated, motor cortex, cortical plasticity, stimulation interval Citation: Yu F, Tang X, Hu R, Liang S, Wang W, Tian S, Wu Y, Yuan T-F and Zhu Y (2021) Corrigendum: The After-Effect of Accelerated Intermittent Theta Burst Stimulation at Different Session Intervals. Front. Neurosci. 15:687972. doi: 10.3389/fnins.2021.687972 Received: 30 March 2021; Accepted: 06 April 2021; Published: 05 May 2021. Edited and reviewed by: Jinhui Wang, South China Normal University, China Copyright © 2021 Yu, Tang, Hu, Liang, Wang, Tian, Wu, Yuan and Zhu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. *Correspondence: Ti-Fei Yuan, [email protected]; Yulian Zhu, [email protected] †These authors have contributed equally to this work and share first authorship
Yanran Li, Bo Sun, Zhanjun Wang, Zhengqing He, Fei Yang, Hongfen Wang, Fang Cui, Zhaohui Chen, Li Ling, ChaoDong Wang, et al.
Frontiers in Neuroscience, Volume 15; doi:10.3389/fnins.2021.595775

Abstract:
Amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease involving the upper and lower motor neurons of the spinal cord, brainstem, and cerebral cortex. At least 30 genes have been implicated in familial ALS (fALS) and sporadic ALS (sALS). Kaneb et al. (2015) first carried out a large-scale sequencing study in ALS patients and identified two loss-of-function (LOF) variants in the GLE1 gene. The LOF mutation-induced disruption of RNA metabolism through the haploinsufficiency mechanism is implicated in ALS pathogenesis. A total of 628 ALS patients and 522 individuals without neurodegenerative disorders were enrolled in this study to explore the GLE1 gene contribution to ALS in the Chinese population. All 16 exons and the flanking intron of GLE1 were screened by Sanger sequencing. In total, we identified seven rare GLE1 coding variants, including one novel nonsense mutation and six rare missense mutations in 628 ALS patients. The frequency of GLE1 LOF mutations was 0.16% (1/628) among Chinese sALS patients, implying that it is an uncommon genetic determinant of ALS in Chinese patients. Additionally, the rare missense variants in the hCG1-binding domain of GLE1 impairing the distribution of the hGle1B isoform at the nuclear pore complex (NPC) region may be involved in the pathogenesis of ALS.
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