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Article ; Online: Real-Time and High-Resolution Monitoring of Neuronal Electrical Activity and pH Variations Based on the Co-Integration of Nanoelectrodes and Chem-FinFETs.

Bettamin, Luca / Mathieu, Fabrice / Marty, Florent H / Blatche, Marie Charline / Gonzalez-Dunia, Daniel / Suberbielle, Elsa / Larrieu, Guilhem

Small (Weinheim an der Bergstrasse, Germany)

2024 , Page(s) e2309055

Abstract: Developing new approaches amenable to the measurement of neuronal physiology in real-time is a very active field of investigation, as it will offer improved methods to assess the impact of diverse insults on neuronal homeostasis. Here, the development of ...

Abstract	Developing new approaches amenable to the measurement of neuronal physiology in real-time is a very active field of investigation, as it will offer improved methods to assess the impact of diverse insults on neuronal homeostasis. Here, the development of an in vitro bio platform is reported which can record the electrical activity of cultured primary rat cortical neurons with extreme sensitivity, while simultaneously tracking the localized changes in the pH of the culture medium. This bio platform features passive vertical nanoprobes with ultra-high signal resolution (several mV amplitude ranges) and Chem-FinFETs (pH sensitivity of sub-0.1 pH units), covering an area as little as a neuronal soma. These multi-sensing units are arranged in an array to probe both chemically and electrically an equivalent surface of ≈ 0.5 mm
Language	English
Publishing date	2024-03-29
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2168935-0
ISSN	1613-6829 ; 1613-6810
ISSN (online)	1613-6829
ISSN	1613-6810
DOI	10.1002/smll.202309055
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity.

Marty, Florent Henri / Bettamin, Luca / Thouard, Anne / Bourgade, Karine / Allart, Sophie / Larrieu, Guilhem / Malnou, Cécile Evelyne / Gonzalez-Dunia, Daniel / Suberbielle, Elsa

iScience

2021 Volume 25, Issue 1, Page(s) 103621

Abstract: Borna disease viruses (BoDV) have recently emerged as zoonotic neurotropic pathogens. These persistent RNA viruses assemble nuclear replication centers (vSPOT) in close interaction with the host chromatin. However, the topology of this interaction and ... ...

Abstract	Borna disease viruses (BoDV) have recently emerged as zoonotic neurotropic pathogens. These persistent RNA viruses assemble nuclear replication centers (vSPOT) in close interaction with the host chromatin. However, the topology of this interaction and its consequences on neuronal function remain unexplored. In neurons, DNA double-strand breaks (DSB) have been identified as novel epigenetic mechanisms regulating neurotransmission and cognition. Activity-dependent DSB contribute critically to neuronal plasticity processes, which could be impaired upon infection. Here, we show that BoDV-1 infection, or the singled-out expression of viral Nucleoprotein and Phosphoprotein, increases neuronal DSB levels. Of interest, inducing DSB promoted the recruitment anew of vSPOT colocalized with DSB and increased viral RNA replication. BoDV-1 persistence decreased neuronal activity and response to stimulation by dampening the surface expression of glutamate receptors. Taken together, our results propose an original mechanistic cross talk between persistence of an RNA virus and neuronal function, through the control of DSB levels.
Language	English
Publishing date	2021-12-16
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.103621
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Article ; Online: Histone acetylation in neuronal (dys)function.

Bonnaud, Emilie M / Suberbielle, Elsa / Malnou, Cécile E

Biomolecular concepts

2016 Volume 7, Issue 2, Page(s) 103–116

Abstract: Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene ...

Abstract	Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene expression. Epigenetic modifications have been shown to play an important role in numerous neuronal functions, from synaptic plasticity to learning and memory. In particular, histone acetylation is a central player in these processes. In this review, we present the molecular mechanisms of histone acetylation and summarize the data underlying the relevance of histone acetylation in cognitive functions in normal and pathological conditions. In the last part, we discuss the different mechanisms underlying the dysregulation of histone acetylation associated with neurological disorders, with a particular focus on environmental causes (stress, drugs, or infectious agents) that are linked to impaired histone acetylation.
MeSH term(s)	Acetylation ; Animals ; Cognition ; Environment ; Epigenesis, Genetic ; Gene Expression Regulation ; Genetic Predisposition to Disease ; Histones/metabolism ; Humans ; Memory ; Mutation ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/metabolism ; Neuronal Plasticity ; Neurons/physiology
Chemical Substances	Histones
Language	English
Publishing date	2016-05-01
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	2557908-3
ISSN	1868-503X ; 1868-5021
ISSN (online)	1868-503X
ISSN	1868-5021
DOI	10.1515/bmc-2016-0002
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Article: Targeting APC-Host Microbe interactions 2Robust control of a neurotropic parasite through MHC I presentation by infected neurons

Salvioni, Anna / Belloy, Marcy / Lebourg, Aurore / Bassot, Emilie / Cantaloube-Ferrieu, Vincent / Vasseur, Virginie / Blanié, Sophie / Liblau, Roland S. / Suberbielle, Elsa / Robey, Ellen A. / Blanchard, Nicolas

Molecular immunology. 2022 Oct., v. 150

2022

Abstract: Control of Central Nervous System (CNS) pathogens by CD8 T cells is pivotal to avoid fatal neuroinflammation. Yet the modalities of MHC I presentation in the brain are poorly understood. We analyzed the antigen presentation mechanisms underlying CD8 T ... ...

Abstract	Control of Central Nervous System (CNS) pathogens by CD8 T cells is pivotal to avoid fatal neuroinflammation. Yet the modalities of MHC I presentation in the brain are poorly understood. We analyzed the antigen presentation mechanisms underlying CD8 T cell-mediated brain restriction of Toxoplasma gondii, a neurotropic parasite that can chronically reside as cysts in the CNS and cause deadly encephalitis. First we engineered transgenic parasites expressing a model antigen that allows the establishment of latent toxoplasmosis in C57BL/6 mice, a mouse model that normally develops encephalitis following T. gondii infection. We show that MHC I presentation of that model antigen suffices to prevent encephalitis, even when restricted to the rapidly dividing tachyzoite stage. We find that improper parasite control in the context of encephalitis correlates with suboptimal MHC I presentation of T. gondii antigens by primary neuronal cultures. Using a new model of conditional MHC I-deficient mice, we finally demonstrate that brain parasite control requires neuronal MHC I presentation. Thus, MHC I presentation by CNS neurons is a crucial checkpoint that determines the clinical outcome of a prevalent and persisting brain infection.
Keywords	Toxoplasma gondii ; antigen presentation ; antigens ; brain ; encephalitis ; genetically modified organisms ; mice ; models ; neurons ; parasites ; tachyzoites ; toxoplasmosis
Language	English
Dates of publication	2022-10
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2022.05.069
Database	NAL-Catalogue (AGRICOLA)

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Zs.A 166: Show issues

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Article ; Online: Histone acetylation in neuronal (dys)function

Bonnaud Emilie M. / Suberbielle Elsa / Malnou Cécile E.

Biomolecular Concepts, Vol 7, Iss 2, Pp 103-

2016 Volume 116

Abstract	Cognitive functions require the expression of an appropriate pattern of genes in response to environmental stimuli. Over the last years, many studies have accumulated knowledge towards the understanding of molecular mechanisms that regulate neuronal gene expression. Epigenetic modifications have been shown to play an important role in numerous neuronal functions, from synaptic plasticity to learning and memory. In particular, histone acetylation is a central player in these processes. In this review, we present the molecular mechanisms of histone acetylation and summarize the data underlying the relevance of histone acetylation in cognitive functions in normal and pathological conditions. In the last part, we discuss the different mechanisms underlying the dysregulation of histone acetylation associated with neurological disorders, with a particular focus on environmental causes (stress, drugs, or infectious agents) that are linked to impaired histone acetylation.
Keywords	cognition ; epigenetics ; histone acetylation ; histone acetyltransferase ; histone deacetylase ; neuron ; synaptic plasticity ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2016-05-01T00:00:00Z
Publisher	De Gruyter
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Borna Disease Virus 1 Phosphoprotein Forms a Tetramer and Interacts with Host Factors Involved in DNA Double-Strand Break Repair and mRNA Processing.

Tarbouriech, Nicolas / Chenavier, Florian / Kawasaki, Junna / Bachiri, Kamel / Bourhis, Jean-Marie / Legrand, Pierre / Freslon, Lily L / Laurent, Estelle M N / Suberbielle, Elsa / Ruigrok, Rob W H / Tomonaga, Keizo / Gonzalez-Dunia, Daniel / Horie, Masayuki / Coyaud, Etienne / Crépin, Thibaut

Viruses

2022 Volume 14, Issue 11

Abstract: Determining the structural organisation of viral replication complexes and unravelling the impact of infection on cellular homeostasis represent important challenges in virology. This may prove particularly useful when confronted with viruses that pose a ...

Abstract	Determining the structural organisation of viral replication complexes and unravelling the impact of infection on cellular homeostasis represent important challenges in virology. This may prove particularly useful when confronted with viruses that pose a significant threat to human health, that appear unique within their family, or for which knowledge is scarce. Among
MeSH term(s)	Animals ; Humans ; Borna disease virus/genetics ; Phosphoproteins/genetics ; Bornaviridae/genetics ; DNA Repair ; DNA ; RNA, Messenger/genetics
Chemical Substances	Phosphoproteins ; DNA (9007-49-2) ; RNA, Messenger
Language	English
Publishing date	2022-10-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14112358
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Borna disease virus docks on neuronal DNA double-strand breaks to replicate and dampens neuronal activity

Florent Henri Marty / Luca Bettamin / Anne Thouard / Karine Bourgade / Sophie Allart / Guilhem Larrieu / Cécile Evelyne Malnou / Daniel Gonzalez-Dunia / Elsa Suberbielle

iScience, Vol 25, Iss 1, Pp 103621- (2022)

2022

Abstract: Summary: Borna disease viruses (BoDV) have recently emerged as zoonotic neurotropic pathogens. These persistent RNA viruses assemble nuclear replication centers (vSPOT) in close interaction with the host chromatin. However, the topology of this ... ...

Abstract	Summary: Borna disease viruses (BoDV) have recently emerged as zoonotic neurotropic pathogens. These persistent RNA viruses assemble nuclear replication centers (vSPOT) in close interaction with the host chromatin. However, the topology of this interaction and its consequences on neuronal function remain unexplored. In neurons, DNA double-strand breaks (DSB) have been identified as novel epigenetic mechanisms regulating neurotransmission and cognition. Activity-dependent DSB contribute critically to neuronal plasticity processes, which could be impaired upon infection. Here, we show that BoDV-1 infection, or the singled-out expression of viral Nucleoprotein and Phosphoprotein, increases neuronal DSB levels. Of interest, inducing DSB promoted the recruitment anew of vSPOT colocalized with DSB and increased viral RNA replication. BoDV-1 persistence decreased neuronal activity and response to stimulation by dampening the surface expression of glutamate receptors. Taken together, our results propose an original mechanistic cross talk between persistence of an RNA virus and neuronal function, through the control of DSB levels.
Keywords	Molecular biology ; Neuroscience ; Virology ; Science ; Q
Subject code	612
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Human Cytomegalovirus Infection Changes the Pattern of Surface Markers of Small Extracellular Vesicles Isolated From First Trimester Placental Long-Term Histocultures.

Bergamelli, Mathilde / Martin, Hélène / Bénard, Mélinda / Ausseil, Jérôme / Mansuy, Jean-Michel / Hurbain, Ilse / Mouysset, Maïlys / Groussolles, Marion / Cartron, Géraldine / Tanguy le Gac, Yann / Moinard, Nathalie / Suberbielle, Elsa / Izopet, Jacques / Tscherning, Charlotte / Raposo, Graça / Gonzalez-Dunia, Daniel / D'Angelo, Gisela / Malnou, Cécile E

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 689122

Abstract: Extracellular vesicles (EVs) have increasingly been recognized as key players in a wide variety of physiological and pathological contexts, including during pregnancy. Notably, EVs appear both as possible biomarkers and as mediators involved in the ... ...

Abstract	Extracellular vesicles (EVs) have increasingly been recognized as key players in a wide variety of physiological and pathological contexts, including during pregnancy. Notably, EVs appear both as possible biomarkers and as mediators involved in the communication of the placenta with the maternal and fetal sides. A better understanding of the physiological and pathological roles of EVs strongly depends on the development of adequate and reliable study models, specifically at the beginning of pregnancy where many adverse pregnancy outcomes have their origin. In this study, we describe the isolation of small EVs from a histoculture model of first trimester placental explants in normal conditions as well as upon infection by human cytomegalovirus. Using bead-based multiplex cytometry and electron microscopy combined with biochemical approaches, we characterized these small EVs and defined their associated markers and ultrastructure. We observed that infection led to changes in the expression level of several surface markers, without affecting the secretion and integrity of small EVs. Our findings lay the foundation for studying the functional role of EVs during early pregnancy, along with the identification of new predictive biomarkers for the severity and outcome of this congenital infection, which are still sorely lacking.
Language	English
Publishing date	2021-09-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.689122
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Article ; Online: Robust Control of a Brain-Persisting Parasite through MHC I Presentation by Infected Neurons.

Salvioni, Anna / Belloy, Marcy / Lebourg, Aurore / Bassot, Emilie / Cantaloube-Ferrieu, Vincent / Vasseur, Virginie / Blanié, Sophie / Liblau, Roland S / Suberbielle, Elsa / Robey, Ellen A / Blanchard, Nicolas

Cell reports

2019 Volume 27, Issue 11, Page(s) 3254–3268.e8

Abstract: Control of CNS pathogens by CD8 T cells is key to avoid fatal neuroinflammation. Yet, the modalities of MHC I presentation in the brain are poorly understood. Here, we analyze the antigen presentation mechanisms underlying CD8 T cell-mediated control of ... ...

Abstract	Control of CNS pathogens by CD8 T cells is key to avoid fatal neuroinflammation. Yet, the modalities of MHC I presentation in the brain are poorly understood. Here, we analyze the antigen presentation mechanisms underlying CD8 T cell-mediated control of the Toxoplasma gondii parasite in the CNS. We show that MHC I presentation of an efficiently processed model antigen (GRA6-OVA), even when not expressed in the bradyzoite stage, reduces cyst burden and dampens encephalitis in C57BL/6 mice. Antigen presentation assays with infected primary neurons reveal a correlation between lower MHC I presentation of tachyzoite antigens by neurons and poor parasite control in vivo. Using conditional MHC I-deficient mice, we find that neuronal MHC I presentation is required for robust restriction of T. gondii in the CNS during chronic phase, showing the importance of MHC I presentation by CNS neurons in the control of a prevalent brain pathogen.
MeSH term(s)	Animals ; Antibodies, Protozoan/immunology ; Antigens, Protozoan/immunology ; Brain/cytology ; Brain/immunology ; Brain/parasitology ; Cell Line ; Cells, Cultured ; Histocompatibility Antigens Class I/genetics ; Histocompatibility Antigens Class I/immunology ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/immunology ; Neurons/parasitology ; Protozoan Proteins/immunology ; Toxoplasma/immunology ; Toxoplasma/pathogenicity ; Toxoplasmosis, Cerebral/immunology
Chemical Substances	Antibodies, Protozoan ; Antigens, Protozoan ; GRA6 protein, Toxoplasma gondii ; Histocompatibility Antigens Class I ; Protozoan Proteins
Language	English
Publishing date	2019-06-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.05.051
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Hippocampal expression of a virus-derived protein impairs memory in mice.

Bétourné, Alexandre / Szelechowski, Marion / Thouard, Anne / Abrial, Erika / Jean, Arnaud / Zaidi, Falek / Foret, Charlotte / Bonnaud, Emilie M / Charlier, Caroline M / Suberbielle, Elsa / Malnou, Cécile E / Granon, Sylvie / Rampon, Claire / Gonzalez-Dunia, Daniel

Proceedings of the National Academy of Sciences of the United States of America

2018 Volume 115, Issue 7, Page(s) 1611–1616

Abstract: The analysis of the biology of neurotropic viruses, notably of their interference with cellular signaling, provides a useful tool to get further insight into the role of specific pathways in the control of behavioral functions. Here, we exploited the ... ...

Abstract	The analysis of the biology of neurotropic viruses, notably of their interference with cellular signaling, provides a useful tool to get further insight into the role of specific pathways in the control of behavioral functions. Here, we exploited the natural property of a viral protein identified as a major effector of behavioral disorders during infection. We used the phosphoprotein (P) of Borna disease virus, which acts as a decoy substrate for protein kinase C (PKC) when expressed in neurons and disrupts synaptic plasticity. By a lentiviral-based strategy, we directed the singled-out expression of P in the dentate gyrus of the hippocampus and we examined its impact on mouse behavior. Mice expressing the P protein displayed increased anxiety and impaired long-term memory in contextual and spatial memory tasks. Interestingly, these effects were dependent on P protein phosphorylation by PKC, as expression of a mutant form of P devoid of its PKC phosphorylation sites had no effect on these behaviors. We also revealed features of behavioral impairment induced by P protein expression but that were independent of its phosphorylation by PKC. Altogether, our findings provide insight into the behavioral correlates of viral infection, as well as into the impact of virus-mediated alterations of the PKC pathway on behavioral functions.
MeSH term(s)	Animals ; Borna Disease/metabolism ; Borna Disease/pathology ; Borna Disease/virology ; Borna disease virus/physiology ; Cells, Cultured ; Cognition Disorders/etiology ; Cognition Disorders/metabolism ; Cognition Disorders/pathology ; Dentate Gyrus/metabolism ; Dentate Gyrus/pathology ; Dentate Gyrus/virology ; Hippocampus/metabolism ; Hippocampus/pathology ; Hippocampus/virology ; Memory, Long-Term/physiology ; Mice ; Mutation ; Neuronal Plasticity ; Neurons/metabolism ; Neurons/pathology ; Neurons/virology ; Phosphoproteins/genetics ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Viral Structural Proteins/genetics ; Viral Structural Proteins/metabolism
Chemical Substances	P protein, Borna disease virus ; Phosphoproteins ; Viral Structural Proteins ; Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2018--13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1711977115
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