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https://www.readbyqxmd.com/read/29674955/the-communication-between-the-immune-and-nervous-systems-the-role-of-il-1%C3%AE-in-synaptopathies
#1
REVIEW
Davide Pozzi, Elisabetta Menna, Alice Canzi, Genni Desiato, Cristina Mantovani, Michela Matteoli
In the last 15 years, groundbreaking genetic progress has underlined a convergence onto coherent synaptic pathways for most psychiatric and neurodevelopmental disorders, which are now collectively called "synaptopathies." However, the modest size of inheritance detected so far indicates a multifactorial etiology for these disorders, underlining the key contribution of environmental effects to them. Inflammation is known to influence the risk and/or severity of a variety of synaptopathies. In particular, pro-inflammatory cytokines, produced and released in the brain by activated astrocytes and microglia, may play a pivotal role in these pathologies...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29668872/microglial-pruning-of-synapses-in-the-prefrontal-cortex-during-adolescence
#2
Allyson P Mallya, Hui-Dong Wang, Han Noo Ri Lee, Ariel Y Deutch
Exaggerated synaptic elimination in the prefrontal cortex (PFC) during adolescence has been suggested to contribute to the neuropathological changes of schizophrenia. Recent data indicate that microglia (MG) sculpt synapses during early postnatal development. However, it is not known if MG contribute to the structural maturation of the PFC, which has a protracted postnatal development. We determined if MG are involved in developmentally specific synapse elimination in the PFC, focusing on adolescence. Layer 5 PFC pyramidal cells (PCs) were intracellularly filled with Lucifer Yellow for dendritic spine measurements in postnatal day (P) 24, P30, P35, P39, and P50 rats...
April 13, 2018: Cerebral Cortex
https://www.readbyqxmd.com/read/29627530/an-enriched-environment-restores-hepatitis-b-vaccination-mediated-impairments-in-synaptic-function-through-ifn-%C3%AE-arginase1-signaling
#3
Fangfang Qi, Zejie Zuo, Saisai Hu, Yucen Xia, Dan Song, Jiechen Kong, Yang Yang, Yingying Wu, Xiao Wang, Junhua Yang, Dandan Hu, Qunfang Yuan, Juntao Zou, Kaihua Guo, Jie Xu, Zhibin Yao
Activation of the neonatal immune system may contribute to deficits in neuronal plasticity. We have reported that neonatal vaccination with a hepatitis B vaccine (HBV) transiently impairs mood status and spatial memory involving a systemic T helper (Th) 2 bias and M1 microglial activation. Here, an EE induced microglial anti-inflammatory M2 polarization, as evidenced by selectively enhanced expression of the Arginase1 gene (Arg-1) in the hippocampus. Interestingly, knock-down of the Arg-1 gene prevented the effects of EE on restoring the dendritic spine density...
April 5, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29581545/microglia-remodel-synapses-by-presynaptic-trogocytosis-and-spine-head-filopodia-induction
#4
Laetitia Weinhard, Giulia di Bartolomei, Giulia Bolasco, Pedro Machado, Nicole L Schieber, Urte Neniskyte, Melanie Exiga, Auguste Vadisiute, Angelo Raggioli, Andreas Schertel, Yannick Schwab, Cornelius T Gross
Microglia are highly motile glial cells that are proposed to mediate synaptic pruning during neuronal circuit formation. Disruption of signaling between microglia and neurons leads to an excess of immature synaptic connections, thought to be the result of impaired phagocytosis of synapses by microglia. However, until now the direct phagocytosis of synapses by microglia has not been reported and fundamental questions remain about the precise synaptic structures and phagocytic mechanisms involved. Here we used light sheet fluorescence microscopy to follow microglia-synapse interactions in developing organotypic hippocampal cultures, complemented by a 3D ultrastructural characterization using correlative light and electron microscopy (CLEM)...
March 26, 2018: Nature Communications
https://www.readbyqxmd.com/read/29574669/microglia-polarization-and-endoplasmic-reticulum-stress-in-chronic-social-defeat-stress-induced-depression-mouse
#5
Jie Tang, Wenbo Yu, Sheng Chen, Zidan Gao, Baoguo Xiao
Inflammation recently has been considered to be participated in the pathogenesis of major depressive disorder (MDD). However, the detailed mechanism of inflammation in depression has not been completely understood yet. In the present study, depression mice model was established by chronic social defeat stress (CSDS) method and confirmed by behavior examinations including forced swimming test and sucrose preference test. The decrease of spine density and postsynaptic density protein 95 (PSD95) in hippocampus further verified the depression model...
March 24, 2018: Neurochemical Research
https://www.readbyqxmd.com/read/29487124/long-term-neuroinflammation-induced-by-influenza-a-virus-infection-and-the-impact-on-hippocampal-neuron-morphology-and-function
#6
Shirin Hosseini, Esther Wilk, Kristin Michaelsen-Preusse, Ingo Gerhauser, Wolfgang Baumgärtner, Robert Geffers, Klaus Schughart, Martin Korte
Acute influenza infection has been reported to be associated with neurological symptoms. However, the long-term consequences for the CNS of an infection with neurotropic but also with non-neurotropic influenza A virus (IAV) variants remain elusive. We can show that spine loss in the hippocampus after infection with neurotropic H7N7 (rSC35M) as well as non-neurotropic H3N2 (maHK68) in female C57BL/6 mice persists well beyond the acute phase of the disease. While spine number was significantly reduced 30 days post infection (pi) with H7N7 or H3N2, full recovery could only be observed much later at 120 days pi...
February 27, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29473218/ngf-steers-microglia-toward-a-neuroprotective-phenotype
#7
Caterina Rizzi, Alexia Tiberi, Michela Giustizieri, Maria Cristina Marrone, Francesco Gobbo, Nicola Maria Carucci, Giovanni Meli, Ivan Arisi, Mara D'Onofrio, Silvia Marinelli, Simona Capsoni, Antonino Cattaneo
Microglia are the sentinels of the brain but a clear understanding of the factors that modulate their activation in physiological and pathological conditions is still lacking. Here we demonstrate that Nerve Growth Factor (NGF) acts on microglia by steering them toward a neuroprotective and anti-inflammatory phenotype. We show that microglial cells express functional NGF receptors in vitro and ex vivo. Our transcriptomic analysis reveals how, in primary microglia, NGF treatment leads to a modulation of motility, phagocytosis and degradation pathways...
February 23, 2018: Glia
https://www.readbyqxmd.com/read/29302779/glia-to-neuron-transfer-of-mirnas-via-extracellular-vesicles-a-new-mechanism-underlying-inflammation-induced-synaptic-alterations
#8
Ilaria Prada, Martina Gabrielli, Elena Turola, Alessia Iorio, Giulia D'Arrigo, Roberta Parolisi, Mariacristina De Luca, Marco Pacifici, Mattia Bastoni, Marta Lombardi, Giuseppe Legname, Dan Cojoc, Annalisa Buffo, Roberto Furlan, Francesca Peruzzi, Claudia Verderio
Recent evidence indicates synaptic dysfunction as an early mechanism affected in neuroinflammatory diseases, such as multiple sclerosis, which are characterized by chronic microglia activation. However, the mode(s) of action of reactive microglia in causing synaptic defects are not fully understood. In this study, we show that inflammatory microglia produce extracellular vesicles (EVs) which are enriched in a set of miRNAs that regulate the expression of key synaptic proteins. Among them, miR-146a-5p, a microglia-specific miRNA not present in hippocampal neurons, controls the expression of presynaptic synaptotagmin1 (Syt1) and postsynaptic neuroligin1 (Nlg1), an adhesion protein which play a crucial role in dendritic spine formation and synaptic stability...
April 2018: Acta Neuropathologica
https://www.readbyqxmd.com/read/29274095/alterations-in-ca1-hippocampal-synapses-in-a-mouse-model-of-fragile-x-syndrome
#9
Safdar Jawaid, Grahame J Kidd, Jing Wang, Carrie Swetlik, Ranjan Dutta, Bruce D Trapp
Fragile X Syndrome (FXS) is the major cause of inherited mental retardation and the leading genetic cause of Autism spectrum disorders. FXS is caused by mutations in the Fragile X Mental Retardation 1 (Fmr1) gene, which results in transcriptional silencing of Fragile X Mental Retardation Protein (FMRP). To elucidate cellular mechanisms involved in the pathogenesis of FXS, we compared dendritic spines in the hippocampal CA1 region of adult wild-type (WT) and Fmr1 knockout (Fmr1-KO) mice. Using diolistic labeling, confocal microscopy, and three-dimensional electron microscopy, we show a significant increase in the diameter of secondary dendrites, an increase in dendritic spine density, and a decrease in mature dendritic spines in adult Fmr1-KO mice...
April 2018: Glia
https://www.readbyqxmd.com/read/29251592/the-role-of-microglia-and-their-cx3cr1-signaling-in-adult-neurogenesis-in-the-olfactory-bulb
#10
Ronen Reshef, Elena Kudryavitskaya, Haran Shani-Narkiss, Batya Isaacson, Neta Rimmerman, Adi Mizrahi, Raz Yirmiya
Microglia play important roles in perinatal neuro- and synapto-genesis. To test the role of microglia in these processes during adulthood, we examined the effects of microglia depletion, via treatment of mice with the CSF-1 receptor antagonist PLX5622, and abrogated neuronal-microglial communication in CX3C receptor-1 deficient ( Cx3cr1-/- ) mice. Microglia depletion significantly lowered spine density in young (developing) but not mature adult-born-granule-cells (abGCs) in the olfactory bulb. Two-photon time-lapse imaging indicated that microglia depletion reduced spine formation and elimination...
December 18, 2017: ELife
https://www.readbyqxmd.com/read/29239126/sexual-dimorphism-of-microglia-and-synapses-during-mouse-postnatal-development
#11
Laetitia Weinhard, Urte Neniskyte, Auguste Vadisiute, Giulia di Bartolomei, Nil Aygün, Laurie Riviere, Francesca Zonfrillo, Susan Dymecki, Cornelius Gross
Microglia participate in synapse remodeling in the cortex and hippocampus during mouse postnatal development. Although sex differences in microglia activity during embryonic development have been reported in these regions, it remains unexplored whether microglia show sexually dimorphic features during the early postnatal period, a critical window for synapse formation and maturation. Here, we investigated morphological and functional features of microglia across early postnatal development as well as morphological features of both pre- and postsynaptic neuronal compartments in the mouse hippocampus...
December 14, 2017: Developmental Neurobiology
https://www.readbyqxmd.com/read/29218848/shank1-is-differentially-expressed-during-development-in-ca1-hippocampal-neurons-and-astrocytes
#12
Sean M Collins, Amogh P Belagodu, Samantha L Reed, Roberto Galvez
Recent studies have strongly suggested a role for the synaptic scaffolding protein SHANK1 in normal synaptic structure and signaling. Global SHANK1 knockout (SHANK1-/-) mice demonstrate reduced dendritic spine density, an immature dendritic spine phenotype and impairments in various cognitive tasks. SHANK1 overexpression is associated with increased dendritic spine size and impairments in fear conditioning. These studies suggest proper regulation of SHANK1 is crucial for appropriate synaptic structure and cognition...
December 8, 2017: Developmental Neurobiology
https://www.readbyqxmd.com/read/29217476/sumo1-impact-on-alzheimer-disease-pathology-in-an-amyloid-depositing-mouse-model
#13
Erin Knock, Shinsuke Matsuzaki, Hironori Takamura, Kanayo Satoh, Grace Rooke, Kyung Han, Hong Zhang, Agnieszka Staniszewski, Taiichi Katayama, Ottavio Arancio, Paul E Fraser
Small ubiquitin-related modifiers (SUMOs) conjugated or bound to target proteins can affect protein trafficking, processing and solubility. SUMOylation has been suggested to play a role in the amyloid plaque and neurofibrillary tangle pathology of Alzheimer disease (AD) and related neurodegenerative diseases. The current study examines the impact of SUMO1 on processing of the amyloid precursor protein (APP) leading to the production and deposition of the amyloid-β (Aβ) peptide. An in vivo model of these pathways was developed by the generation of double transgenic mice over-expressing human SUMO1 and a mutant APP...
February 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29133437/abnormal-microglia-and-enhanced-inflammation-related-gene-transcription-in-mice-with-conditional-deletion-of-ctcf-in-camk2a-cre-expressing-neurons
#14
Bryan E McGill, Ruteja A Barve, Susan E Maloney, Amy Strickland, Nicholas Rensing, Peter L Wang, Michael Wong, Richard Head, David F Wozniak, Jeffrey Milbrandt
CCCTC-binding factor (CTCF) is an 11 zinc finger DNA-binding domain protein that regulates gene expression by modifying 3D chromatin structure. Human mutations in CTCF cause intellectual disability and autistic features. Knocking out Ctcf in mouse embryonic neurons is lethal by neonatal age, but the effects of CTCF deficiency in postnatal neurons are less well studied. We knocked out Ctcf postnatally in glutamatergic forebrain neurons under the control of Camk2a-Cre. Ctcf loxP/loxP ; Camk2a-Cre + ( Ctcf CKO) mice of both sexes were viable and exhibited profound deficits in spatial learning/memory, impaired motor coordination, and decreased sociability by 4 months of age...
January 3, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29078046/dendritic-polyglycerol-sulfates-in-the-prevention-of-synaptic-loss-and-mechanism-of-action-on-glia
#15
Dusica Maysinger, Jeff Ji, Alexandre Moquin, Shireen Hossain, Mark A Hancock, Issan Zhang, Philip K Y Chang, Matthew Rigby, Madeleine Anthonisen, Peter Grutter, John C S Breitner, R Anne McKinney, Sabine Reimann, Rainer Haag, Gerhard Multhaup
Dendritic polyglycerols (dPG), particularly dendritic polyglycerol sulfates (dPGS), have been intensively studied due to their intrinsic anti-inflammatory activity. As related to brain pathologies involving neuroinflammation, the current study examined if dPG and dPGS can (i) regulate neuroglial activation, and (ii) normalize the morphology and function of excitatory postsynaptic dendritic spines adversely affected by the neurotoxic 42 amino acid amyloid-β (Aβ42) peptide of Alzheimer disease (AD). The exact role of neuroglia, such as microglia and astrocytes, remains controversial especially their positive and negative impact on inflammatory processes in AD...
October 27, 2017: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/29017970/absence-of-microglial-cx3cr1-impairs-the-synaptic-integration-of-adult-born-hippocampal-granule-neurons
#16
M Bolós, J R Perea, J Terreros-Roncal, N Pallas-Bazarra, J Jurado-Arjona, J Ávila, M Llorens-Martín
Microglia are immune cells that play a crucial role in maintaining brain homeostasis. Among the mechanisms of communication between microglia and neurons, the CX3CL1/CX3CR1 axis exerts a central modulatory role. Animals lacking CX3CR1 microglial receptor (CX3CR1-/- mice) exhibit marked alterations not only in microglia but also in neurons located in various regions of the brain. Here we show that microglial depletion of CX3CR1 leads to the deficient synaptic integration of adult-born granule neurons in the dentate gyrus (DG), both at the afferent and efferent level...
February 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28948967/corticostriatal-circuit-defects-in-hoxb8-mutant-mice
#17
N Nagarajan, B W Jones, P J West, R E Marc, M R Capecchi
Hoxb8 mutant mice exhibit compulsive grooming and hair removal dysfunction similar to humans with the obsessive-compulsive disorder (OCD)-spectrum disorder, trichotillomania. As, in the mouse brain, the only detectable cells that label with Hoxb8 cell lineage appear to be microglia, we suggested that defective microglia cause the neuropsychiatric disorder. Does the Hoxb8 mutation in microglia lead to neural circuit dysfunctions? We demonstrate that Hoxb8 mutants contain corticostriatal circuit defects. Golgi staining, ultra-structural and electrophysiological studies of mutants reveal excess dendritic spines, pre- and postsynaptic structural defects, long-term potentiation and miniature postsynaptic current defects...
September 26, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28771976/hdac3-negatively-regulates-spatial-memory-in-a-mouse-model-of-alzheimer-s-disease
#18
Xiaolei Zhu, Sulei Wang, Linjie Yu, Jiali Jin, Xing Ye, Yi Liu, Yun Xu
The accumulation and deposition of beta-amyloid (Aβ) is a key neuropathological hallmark of Alzheimer's disease (AD). Histone deacetylases (HDACs) are promising therapeutic targets for the treatment of AD, while the specific HDAC isoforms associated with cognitive improvement are poorly understood. In this study, we investigate the role of HDAC3 in the pathogenesis of AD. Nuclear HDAC3 is significantly increased in the hippocampus of 6- and 9-month-old APPswe/PS1dE9 (APP/PS1) mice compared with that in age-matched wild-type C57BL/6 (B6) mice...
October 2017: Aging Cell
https://www.readbyqxmd.com/read/28729191/hypothermia-pretreatment-improves-cognitive-impairment-via-enhancing-synaptic-plasticity-in-a-traumatic-brain-injury-model
#19
Bingjin Liu, Lin Wang, Yun Cao, Weiqi Xu, Fangxiao Shi, Qing Tian, Xinwen Zhou
PosttraumatichypothermiaattenuatescognitivedeficitscausedbyTBIwhen it is administered at an early stage. However, little is known regarding the effect of hypothermia pretreatment on cognitive deficits one month after TBI. In the current study, the behavior test revealed that hypothermia pretreatment mitigates the learning and memory impairment induced by TBI in mice. Hypothermia treatment significantly increased the expression of PSD93, PSD95 and NR2B one month after TBI in the cortex and hippocampus compared with the normothermia group...
July 17, 2017: Brain Research
https://www.readbyqxmd.com/read/28697890/stress-induced-neuronal-colony-stimulating-factor-1-provokes-microglia-mediated-neuronal-remodeling-and-depressive-like-behavior
#20
Eric S Wohleb, Rosemarie Terwilliger, Catharine H Duman, Ronald S Duman
BACKGROUND: Chronic stress exposure causes neuronal atrophy and synaptic deficits in the medial prefrontal cortex (PFC), contributing to development of anxiety- and depressive-like behaviors. Concomitantly, microglia in the PFC undergo morphological and functional changes following stress exposure, suggesting that microglia contribute to synaptic deficits underlying behavioral consequences. METHODS: Male and female mice were exposed to chronic unpredictable stress (CUS) to examine the role of neuron-microglia interactions in the medial PFC during development of anxiety- and depressive-like behaviors...
January 1, 2018: Biological Psychiatry
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