TY - JOUR AU - Hencz, Alexandra Júlia AU - Magony, Andor Dániel AU - Thomas, Chloe AU - Kovacs, Krisztina AU - Szilágyi, Tamás Gábor AU - Pál, József AU - Sík, Attila TI - Short-term hyperoxia-induced functional and morphological changes in rat hippocampus JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 PG - 13 SN - 1662-5102 DO - 10.3389/fncel.2024.1376577 UR - https://m2.mtmt.hu/api/publication/34836454 ID - 34836454 N1 - * Megosztott szerzőség AB - Excess oxygen (O2) levels may have a stimulating effect, but in the long term, and at high concentrations of O2, it is harmful to the nervous system. The hippocampus is very sensitive to pathophysiological changes and altered O2 concentrations can interfere with hippocampus-dependent learning and memory functions. In this study, we investigated the hyperoxia-induced changes in the rat hippocampus to evaluate the short-term effect of mild and severe hyperoxia. Wistar male rats were randomly divided into control (21% O2), mild hyperoxia (30% O2), and severe hyperoxia groups (100% O2). The O2 exposure lasted for 60 min. Multi-channel silicon probes were used to study network oscillations and firing properties of hippocampal putative inhibitory and excitatory neurons. Neural damage was assessed using the Gallyas silver impregnation method. Mild hyperoxia (30% O2) led to the formation of moderate numbers of silver-impregnated "dark" neurons in the hippocampus. On the other hand, exposure to 100% O2 was associated with a significant increase in the number of "dark" neurons located mostly in the hilus. The peak frequency of the delta oscillation decreased significantly in both mild and severe hyperoxia in urethane anesthetized rats. Compared to normoxia, the firing activity of pyramidal neurons under hyperoxia increased while it was more heterogeneous in putative interneurons in the cornu ammonis area 1 (CA1) and area 3 (CA3). These results indicate that short-term hyperoxia can change the firing properties of hippocampal neurons and network oscillations and damage neurons. Therefore, the use of elevated O2 concentration inhalation in hospitals (i.e., COVID treatment and surgery) and in various non-medical scenarios (i.e., airplane emergency O2 masks, fire-fighters, and high altitude trekkers) must be used with extreme caution. LA - English DB - MTMT ER - TY - JOUR AU - Fesharaki-Zadeh, Arman AU - Datta, Dibyadeep TI - An overview of preclinical models of traumatic brain injury (TBI): relevance to pathophysiological mechanisms JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SP - 1 EP - 19 PG - 19 SN - 1662-5102 DO - 10.3389/fncel.2024.1371213 UR - https://m2.mtmt.hu/api/publication/34825127 ID - 34825127 LA - English DB - MTMT ER - TY - JOUR AU - Mishima, T. AU - Komano, K. AU - Tabaru, M. AU - Kofuji, T. AU - Saito, A. AU - Ugawa, Y. AU - Terao, Y. TI - Repetitive pulsed-wave ultrasound stimulation suppresses neural activity by modulating ambient GABA levels via effects on astrocytes JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1361242 UR - https://m2.mtmt.hu/api/publication/34815337 ID - 34815337 N1 - Department of Medical Physiology, Kyorin University School of Medicine, Mitaka, Japan Institute of Innovative Research, Tokyo Institute of Technology, Yokohama, Japan Radioisotope Laboratory, Kyorin University School of Medicine, Mitaka, Japan Department of Human Neurophysiology, School of Medicine, Fukushima Medical University, Fukushima, Japan Export Date: 23 April 2024 Correspondence Address: Mishima, T.; Department of Medical Physiology, Japan; email: mishimat@ks.kyorin-u.ac.jp Correspondence Address: Terao, Y.; Department of Medical Physiology, Japan; email: yterao@ks.kyorin-u.ac.jp LA - English DB - MTMT ER - TY - JOUR AU - Engler-Chiurazzi, Elizabeth TI - B cells and the stressed brain: emerging evidence of neuroimmune interactions in the context of psychosocial stress and major depression JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SP - 1 EP - 21 PG - 21 SN - 1662-5102 DO - 10.3389/fncel.2024.1360242 UR - https://m2.mtmt.hu/api/publication/34814733 ID - 34814733 AB - The immune system has emerged as a key regulator of central nervous system (CNS) function in health and in disease. Importantly, improved understanding of immune contributions to mood disorders has provided novel opportunities for the treatment of debilitating stress-related mental health conditions such as major depressive disorder (MDD). Yet, the impact to, and involvement of, B lymphocytes in the response to stress is not well-understood, leaving a fundamental gap in our knowledge underlying the immune theory of depression. Several emerging clinical and preclinical findings highlight pronounced consequences for B cells in stress and MDD and may indicate key roles for B cells in modulating mood. This review will describe the clinical and foundational observations implicating B cell-psychological stress interactions, discuss potential mechanisms by which B cells may impact brain function in the context of stress and mood disorders, describe research tools that support the investigation of their neurobiological impacts, and highlight remaining research questions. The goal here is for this discussion to illuminate both the scope and limitations of our current understanding regarding the role of B cells, stress, mood, and depression. LA - English DB - MTMT ER - TY - JOUR AU - Faralli, A. AU - Fucà, E. AU - Lazzaro, G. AU - Menghini, D. AU - Vicari, S. AU - Costanzo, F. TI - Transcranial Direct Current Stimulation in neurogenetic syndromes: new treatment perspectives for Down syndrome? JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1328963 UR - https://m2.mtmt.hu/api/publication/34802268 ID - 34802268 N1 - Child and Adolescent Neuropsychiatry Unit, Bambino Gesù Children's Hospital (IRCCS), Rome, Italy Life Sciences and Public Health Department, Catholic University of Sacred Heart, Rome, Italy Export Date: 21 April 2024 Correspondence Address: Costanzo, F.; Child and Adolescent Neuropsychiatry Unit, Italy; email: floriana.costanzo@opbg.net Chemicals/CAS: glutamic acid, 11070-68-1, 138-15-8, 56-86-0, 6899-05-4 Funding details: Ministero della Salute Funding text 1: The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported also by the Italian Ministry of Health with Current Research Funds. AB - This perspective review aims to explore the potential neurobiological mechanisms involved in the application of transcranial Direct Current Stimulation (tDCS) for Down syndrome (DS), the leading cause of genetically-based intellectual disability. The neural mechanisms underlying tDCS interventions in genetic disorders, typically characterized by cognitive deficits, are grounded in the concept of brain plasticity. We initially present the neurobiological and functional effects elicited by tDCS applications in enhancing neuroplasticity and in regulating the excitatory/inhibitory balance, both associated with cognitive improvement in the general population. The review begins with evidence on tDCS applications in five neurogenetic disorders, including Rett, Prader-Willi, Phelan-McDermid, and Neurofibromatosis 1 syndromes, as well as DS. Available evidence supports tDCS as a potential intervention tool and underscores the importance of advancing neurobiological research into the mechanisms of tDCS action in these conditions. We then discuss the potential of tDCS as a promising non-invasive strategy to mitigate deficits in plasticity and promote fine-tuning of the excitatory/inhibitory balance in DS, exploring implications for cognitive treatment perspectives in this population. Copyright © 2024 Faralli, Fucà, Lazzaro, Menghini, Vicari and Costanzo. LA - English DB - MTMT ER - TY - JOUR AU - Tieck, M.P. AU - Vasilenko, N. AU - Ruschil, C. AU - Kowarik, M.C. TI - Peripheral memory B cells in multiple sclerosis vs. double negative B cells in neuromyelitis optica spectrum disorder: disease driving B cell subsets during CNS inflammation JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1337339 UR - https://m2.mtmt.hu/api/publication/34780924 ID - 34780924 N1 - Export Date: 10 April 2024 Correspondence Address: Kowarik, M.C.; Department of Neurology and Stroke, Germany; email: markus.kowarik@uni-tuebingen.de Chemicals/CAS: alemtuzumab, 216503-57-0; dimethyl fumarate, 624-49-7; epithelial derived neutrophil activating factor 78, 136956-40-6; glatiramer, 147245-92-9, 28704-27-0; infliximab, 170277-31-3; natalizumab, 189261-10-7; ocrelizumab, 637334-45-3; rituximab, 174722-31-7 Funding text 1: The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article. AB - B cells are fundamental players in the pathophysiology of autoimmune diseases of the central nervous system, such as multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). A deeper understanding of disease-specific B cell functions has led to the differentiation of both diseases and the development of different treatment strategies. While NMOSD is strongly associated with pathogenic anti-AQP4 IgG antibodies and proinflammatory cytokine pathways, no valid autoantibodies have been identified in MS yet, apart from certain antigen targets that require further evaluation. Although both diseases can be effectively treated with B cell depleting therapies, there are distinct differences in the peripheral B cell subsets that influence CNS inflammation. An increased peripheral blood double negative B cells (DN B cells) and plasmablast populations has been demonstrated in NMOSD, but not consistently in MS patients. Furthermore, DN B cells are also elevated in rheumatic diseases and other autoimmune entities such as myasthenia gravis and Guillain-Barré syndrome, providing indirect evidence for a possible involvement of DN B cells in other autoantibody-mediated diseases. In MS, the peripheral memory B cell pool is affected by many treatments, providing indirect evidence for the involvement of memory B cells in MS pathophysiology. Moreover, it must be considered that an important effector function of B cells in MS may be the presentation of antigens to peripheral immune cells, including T cells, since B cells have been shown to be able to recirculate in the periphery after encountering CNS antigens. In conclusion, there are clear differences in the composition of B cell populations in MS and NMOSD and treatment strategies differ, with the exception of broad B cell depletion. This review provides a detailed overview of the role of different B cell subsets in MS and NMOSD and their implications for treatment options. Specifically targeting DN B cells and plasmablasts in NMOSD as opposed to memory B cells in MS may result in more precise B cell therapies for both diseases. Copyright © 2024 Tieck, Vasilenko, Ruschil and Kowarik. LA - English DB - MTMT ER - TY - JOUR AU - Inavalli, V.V.G.K. AU - Puente, Muñoz V. AU - Draffin, J.E. AU - Tønnesen, J. TI - Fluorescence microscopy shadow imaging for neuroscience JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1330100 UR - https://m2.mtmt.hu/api/publication/34769175 ID - 34769175 N1 - Center for Cancer Immunology, University of Southampton, Southampton, United Kingdom Department of Neurosciences, Faculty of Medicine and Nursing, University of the Basque Country (UPV/EHU), Leioa, Spain Neuronal Excitability Lab, Achucarro Basque Center for Neuroscience, Leioa, Spain Aligning Science Across Parkinson’s (ASAP), Collaborative Research Network, Chevy ChaseMD, United States Instituto Biofisika (CSIC/UPV), Leioa, Spain Export Date: 4 April 2024 Correspondence Address: Tønnesen, J.; Department of Neurosciences, Spain; email: tonnesen@csic.es Funding details: 101067304 Funding details: National Science Foundation, NSF Funding details: National Institutes of Health, NIH Funding details: Euskal Herriko Unibertsitatea, EHU, ASAP-020505, GIU21/048 Funding details: Ministerio de Ciencia e Innovación, MICINN, PCI2022-135040-2, PID2020-113894RB-I00 Funding details: Agencia Estatal de Investigación, AEI Funding text 1: The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The authors acknowledge funding for their general work from the Spanish Ministry of Science and Innovation (Grant PID2020-113894RB-I00), Project (PCI2022-135040-2) funded by the Spanish State Research Agency through PCI, as part of the AEI/NSF/NIH Collaborative Research in Computational Neuroscience program, and from the University of the Basque Country (Grant GIU21/048). This research was funded in whole or in part by Aligning Science Across Parkinson’s ASAP-020505 through the Michael J. Fox Foundation for Parkinson’s Research (MJFF). For the purpose of open access, the authors have applied a CC BY public copyright license to all authors Accepted Manuscripts arising from this submission. VP is a Marie Skłodowska Curie Fellow funded through the the European Union’s Horizon Europe research and innovation programme grant agreement (101067304, NeuroExcell). AB - Fluorescence microscopy remains one of the single most widely applied experimental approaches in neuroscience and beyond and is continuously evolving to make it easier and more versatile. The success of the approach is based on synergistic developments in imaging technologies and fluorophore labeling strategies that have allowed it to greatly diversify and be used across preparations for addressing structure as well as function. Yet, while targeted labeling strategies are a key strength of fluorescence microscopy, they reciprocally impose general limitations on the possible types of experiments and analyses. One recent development that overcomes some of these limitations is fluorescence microscopy shadow imaging, where membrane-bound cellular structures remain unlabeled while the surrounding extracellular space is made to fluoresce to provide a negative contrast shadow image. When based on super-resolution STED microscopy, the technique in effect provides a positive image of the extracellular space geometry and entire neuropil in the field of view. Other noteworthy advantages include the near elimination of the adverse effects of photobleaching and toxicity in live imaging, exhaustive and homogeneous labeling across the preparation, and the ability to apply and adjust the label intensity on the fly. Shadow imaging is gaining popularity and has been applied on its own or combined with conventional positive labeling to visualize cells and synaptic proteins in their parenchymal context. Here, we highlight the inherent limitations of fluorescence microscopy and conventional labeling and contrast these against the pros and cons of recent shadow imaging approaches. Our aim is to describe the brief history and current trajectory of the shadow imaging technique in the neuroscience field, and to draw attention to its ease of application and versatility. Copyright © 2024 Inavalli, Puente Muñoz, Draffin and Tønnesen. LA - English DB - MTMT ER - TY - JOUR AU - Li, Z. AU - Wu, J. AU - Zhao, T. AU - Wei, Y. AU - Xu, Y. AU - Liu, Z. AU - Li, X. AU - Chen, X. TI - Microglial activation in spaceflight and microgravity: potential risk of cognitive dysfunction and poor neural health JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1296205 UR - https://m2.mtmt.hu/api/publication/34766165 ID - 34766165 N1 - Beijing International Science and Technology Cooperation Base for Antiviral Drugs, College of Chemistry and Life Science, Beijing University of Technology, Beijing, China Department of Rehabilitation, Beijing Rehabilitation Hospital, Capital Medical University, Beijing, China School of Life Sciences, Beijing Institute of Technology, Beijing, China Export Date: 3 April 2024 Correspondence Address: Chen, X.; Beijing International Science and Technology Cooperation Base for Antiviral Drugs, China; email: chenxuechai@bjut.edu.cn Correspondence Address: Liu, Z.; Department of Rehabilitation, China; email: liuzj888@ccmu.edu.cn Correspondence Address: Li, X.; School of Life Sciences, China; email: aeople@126.com Funding details: KM202010005022 Funding details: National Natural Science Foundation of China, NSFC, 82271283 Funding details: Natural Science Foundation of Beijing Municipality, 7202001 Funding text 1: The authors declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from the National Natural Science Foundation of China (No. 82271283), the Natural Science Foundation of Beijing Municipality (No. 7202001), and the Scientific Research Project of the Beijing Educational Committee (No. KM202010005022). AB - Due to the increased crewed spaceflights in recent years, it is vital to understand how the space environment affects human health. A lack of gravitational force is known to risk multiple physiological functions of astronauts, particularly damage to the central nervous system (CNS). As innate immune cells of the CNS, microglia can transition from a quiescent state to a pathological state, releasing pro-inflammatory cytokines that contribute to neuroinflammation. There are reports indicating that microglia can be activated by simulating microgravity or exposure to galactic cosmic rays (GCR). Consequently, microglia may play a role in the development of neuroinflammation during spaceflight. Prolonged spaceflight sessions raise concerns about the chronic activation of microglia, which could give rise to various neurological disorders, posing concealed risks to the neural health of astronauts. This review summarizes the risks associated with neural health owing to microglial activation and explores the stressors that trigger microglial activation in the space environment. These stressors include GCR, microgravity, and exposure to isolation and stress. Of particular focus is the activation of microglia under microgravity conditions, along with the proposal of a potential mechanism. Copyright © 2024 Li, Wu, Zhao, Wei, Xu, Liu, Li and Chen. LA - English DB - MTMT ER - TY - JOUR AU - Bobotis, B.C. AU - Halvorson, T. AU - Carrier, M. AU - Tremblay, M.-È. TI - Established and emerging techniques for the study of microglia: visualization, depletion, and fate mapping JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1317125 UR - https://m2.mtmt.hu/api/publication/34766164 ID - 34766164 N1 - Division of Medical Sciences, University of Victoria, Victoria, BC, Canada Centre for Advanced Materials and Related Technology, Victoria, BC, Canada Department of Medicine, University of British Columbia, Vancouver, BC, Canada Department of Surgery, University of British Columbia, Vancouver, BC, Canada British Columbia Children’s Hospital Research Institute, Vancouver, BC, Canada Département de Psychiatrie et de Neurosciences, Faculté de Médecine, Université Laval, Québec City, QC, Canada Axe neurosciences, Centre de Recherche du CHU de Québec, Université Laval, Québec City, QC, Canada Department of Molecular Medicine, Université Laval, Québec City, QC, Canada Export Date: 3 April 2024 Correspondence Address: Tremblay, M.-È.; Division of Medical Sciences, Canada Chemicals/CAS: colony stimulating factor 1, 81627-83-0; gelatinase A, 146480-35-5; gelatinase B, 146480-36-6; protein tyrosine phosphatase; receptor type tyrosine protein phosphatase C Funding details: Canadian Institutes of Health Research, IRSC Funding details: Fonds de Recherche du Québec - Santé, FRQS Funding details: Royal Society of Canada, RSC Funding details: International Development Research Centre, IDRC, 109925 Funding details: Canada Research Chairs Funding details: University of British Columbia, UBC Funding text 1: The authors declare financial support was received for the research, authorship, and/or publication of this article. This work was carried out with the aid of a grant from the International Development Research Centre (IDRC; project ID 109925). BB was supported by a master award from the Division of Medical Sciences at University of Victoria. TH was supported by a British Columbia Children’s Hospital Research Institute Doctoral Award and the University of British Columbia MD/Ph.D. program. MC was supported by a doctoral training award from Fonds de Recherche du Québec–Santé. This work was supported by research grants from CIHR awarded to M-ÈT., who was a College Member of the Royal Society of Canada and a Canada Research Chair (Tier II) in Neurobiology of Aging and Cognition. AB - The central nervous system (CNS) is an essential hub for neuronal communication. As a major component of the CNS, glial cells are vital in the maintenance and regulation of neuronal network dynamics. Research on microglia, the resident innate immune cells of the CNS, has advanced considerably in recent years, and our understanding of their diverse functions continues to grow. Microglia play critical roles in the formation and regulation of neuronal synapses, myelination, responses to injury, neurogenesis, inflammation, and many other physiological processes. In parallel with advances in microglial biology, cutting-edge techniques for the characterization of microglial properties have emerged with increasing depth and precision. Labeling tools and reporter models are important for the study of microglial morphology, ultrastructure, and dynamics, but also for microglial isolation, which is required to glean key phenotypic information through single-cell transcriptomics and other emerging approaches. Strategies for selective microglial depletion and modulation can provide novel insights into microglia-targeted treatment strategies in models of neuropsychiatric and neurodegenerative conditions, cancer, and autoimmunity. Finally, fate mapping has emerged as an important tool to answer fundamental questions about microglial biology, including their origin, migration, and proliferation throughout the lifetime of an organism. This review aims to provide a comprehensive discussion of these established and emerging techniques, with applications to the study of microglia in development, homeostasis, and CNS pathologies. Copyright © 2024 Bobotis, Halvorson, Carrier and Tremblay. LA - English DB - MTMT ER - TY - JOUR AU - Boland, R. AU - Kokiko-Cochran, O.N. TI - Deplete and repeat: microglial CSF1R inhibition and traumatic brain injury JF - FRONTIERS IN CELLULAR NEUROSCIENCE J2 - FRONT CELL NEUROSCI VL - 18 PY - 2024 SN - 1662-5102 DO - 10.3389/fncel.2024.1352790 UR - https://m2.mtmt.hu/api/publication/34766161 ID - 34766161 N1 - Export Date: 3 April 2024 Correspondence Address: Kokiko-Cochran, O.N.; Department of Neuroscience, United States; email: olga.kokiko-cochran@osumc.edu Chemicals/CAS: aquaporin 4, 175960-54-0; cannabidiol, 13956-29-1; caspase 11, 216503-96-7; clodronic acid, 10596-23-3, 22560-50-5; colony stimulating factor 1, 81627-83-0; curcumin, 458-37-7; minocycline, 10118-90-8, 11006-27-2, 13614-98-7; n sec butyl 1 (2 chlorophenyl) n methyl 3 isoquinolinecarboxamide, 85532-75-8; pexidartinib, 1029044-16-3, 2040295-03-0; sotuletinib, 953769-46-5 Funding details: National Institute of Neurological Disorders and Stroke, NINDS, R01NS109585 Funding text 1: The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by a NINDS R01NS109585 to OK-C. AB - Traumatic brain injury (TBI) is a public health burden affecting millions of people. Sustained neuroinflammation after TBI is often associated with poor outcome. As a result, increased attention has been placed on the role of immune cells in post-injury recovery. Microglia are highly dynamic after TBI and play a key role in the post-injury neuroinflammatory response. Therefore, microglia represent a malleable post-injury target that could substantially influence long-term outcome after TBI. This review highlights the cell specific role of microglia in TBI pathophysiology. Microglia have been manipulated via genetic deletion, drug inhibition, and pharmacological depletion in various pre-clinical TBI models. Notably, colony stimulating factor 1 (CSF1) and its receptor (CSF1R) have gained much traction in recent years as a pharmacological target on microglia. CSF1R is a transmembrane tyrosine kinase receptor that is essential for microglia proliferation, differentiation, and survival. Small molecule inhibitors targeting CSF1R result in a swift and effective depletion of microglia in rodents. Moreover, discontinuation of the inhibitors is sufficient for microglia repopulation. Attention is placed on summarizing studies that incorporate CSF1R inhibition of microglia. Indeed, microglia depletion affects multiple aspects of TBI pathophysiology, including neuroinflammation, oxidative stress, and functional recovery with measurable influence on astrocytes, peripheral immune cells, and neurons. Taken together, the data highlight an important role for microglia in sustaining neuroinflammation and increasing risk of oxidative stress, which lends to neuronal damage and behavioral deficits chronically after TBI. Ultimately, the insights gained from CSF1R depletion of microglia are critical for understanding the temporospatial role that microglia develop in mediating TBI pathophysiology and recovery. Copyright © 2024 Boland and Kokiko-Cochran. LA - English DB - MTMT ER -