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Glial Cells: Managers of Neuro-immunity

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198351 Year: Pages: 224 DOI: 10.3389/978-2-88919-835-1 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-01-19 14:05:46
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Immune responses within the brain are still scarcely explored. Nerve tissue damage is accompanied by the activation of glial cells, primarily microglia and astroglia, and such activation is responsible for the release of cytokines and chemokines that maintain the local inflammatory response and actively recruit lymphocytes and monocytes to the damaged areas. Theoretically, these responses are designed to repair the brain damage. However, alterations, or a chronic perpetuation of these responses may underlie a number of neuro-pathologies. It is thought that each inflammatory scenario within the brain have a specific biochemical footprint characterized by the release of determined cytokines, chemokines and growing factors able to define particular immunological responses. Alongside, glial cells transform their cell body, become larger and develop higher number of branches adopting an active morphological phenotype. These changes are related with the search of interactions with other cells, such as bystander resident cells of the brain parenchyma, but also cells homing from the blood stream. In this process, microglia and astrocytes communicates with other cells by the formation of specific intercellular connections that are still poorly understood. These interactions are complex and entail the arrangement of cytoskeletal compounds, secretory and phagocytic domains. In this particular crosstalk there is a two-way communication in which glial cells and target cells come together establishing interfaces with specific information exchange. This way, glial cells orchestrate the particular response recruiting cellular subsets within the central nervous system and organizing the resolution of the brain damage. In this Frontiers Research Topic, we compile a selection of articles unfolding diverse aspects of glial-derived inflammation, focused on neurodegenerative diseases and other nervous system disorders, with special emphasis on microglia/macrophages as leading actors managing neuro-immunity.

Glial Plasticity in Depression

Authors: --- --- --- --- et al.
Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199990 Year: Pages: 99 DOI: 10.3389/978-2-88919-999-0 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-01-19 14:05:46
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Major depression is a highly prevalent disorder that poses a significant social burden in society nowadays. The pathophysiology of this disease is still poorly understood but growing evidence suggests that impaired neuron and glial plasticity may be a key underlying mechanism for the precipitation of the disorder. One of the most surprising findings in this field was the involvement of glial cells in the pathophysiology of major depression and in the action of antidepressants, namely in mechanisms related with adult neurogenesis imbalances or dendritic arborization impairments. In particular, several works refer to alterations in the morphology and numbers of astrocytes, microglia and oligodendrocytes in the context of depression in human patients or animal models of depression. These observations were linked to functional evidences and suggested to underlie the pathophysiology of depression. Among others, these include impairments in the cross-talk between glia and neurons, changes in the level of neurotransmitter or immunoactive substances, myelination status, synapse formation, maintenance, or elimination. In addition to the implication of glia in the pathophysiology of depression, a number of studies is ascribing glia pathways to classically accepted antidepressant mechanisms. Therefore, it is noteworthy to elucidate the role of glia in the effect provided by antidepressant treatment in order to better understand secondary effects and elucidate alternative targets for treatment.

Single Membrane Channels Formed by Connexins or Pannexins: Focus on the Nervous System

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889198900 Year: Pages: 241 DOI: 10.3389/978-2-88919-890-0 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-01-19 14:05:46
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Given that the extremely elaborated and dynamic functions performed by the nervous system require the close synchronization of brain cells, complex organisms have developed different mechanisms of intercellular communication. At this regard, paracrine signaling between neighboring cells is currently recognized as one of the most widely distributed mechanisms of synchronization in the brain parenchyma. In mammals, paracrine signaling is in part mediated by single membrane channels formed by connexins (connexons/hemichannels) or pannexins (pannexons), which are two different membrane protein families composed of about 20 and 3 members, respectively. Single membrane channels formed by these proteins serve as aqueous pores permeable to ions and small molecules, allowing the diffusional exchange between the intra- and extracellular milieu. Thus, connexin hemichannels and pannexons permit the release of significant quantities of autocrine/paracrine signaling molecules (e.g., ATP, glutamate, NAD+, adenosine and PGE2) into the extracellular milieu, as well as the uptake of small molecules. An increasing body of evidence has revealed that connexin hemichannels and pannexons play a crucial role in a plethora of brain processes including blood flow regulation, Ca2+ wave propagation, memory consolidation, glucose sensing and cell migration and adhesion. Considering the multiple cell signaling functions of these channels, their dysregulation is proposed not only as potential pathological biomarker, but it has been implicated in the pathogenesis and progression of diverse brain diseases (e.g., meningitis, Alzheimer’s disease and stroke). The aim of this Research Topic is to gather a collection of original research articles, method, protocols, short communications, opinions, perspectives, as well as review articles, providing the latest progress and insights in the field of connexin hemichannels and pannexons in the nervous system. Within this volume we plan to cover from basic research including channel structure, regulation, pharmacology and trafficking; to different biological functions in the physiology (behavior, plasticity, neurogenesis, blood flow control, neuron-glia crosstalk, cell migration and differentiation) as well as in the pathophysiology (neuroinflammation, mutation-related diseases, glial dysfunction and neurodegeneration) of the nervous system. We hope that this collection of articles will serve to understand how the signaling of connexin hemichannels and pannexons influences both normal and pathological brain function.

Keywords

astrocyte --- Microglia --- Neuron --- Brain --- glia --- connexin --- pannexin --- hemichannel --- connexon --- pannexon

Cytokines as Players of Neuronal Plasticity and Sensitivity to Environment in Healthy and Pathological Brain

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197682 Year: Pages: 158 DOI: 10.3389/978-2-88919-768-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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It is now accepted that immune molecules are not only present within the brain during pathology but they exert physiological functions in the "healthy" brain as well. Increasing evidence points to a neuro-modulatory role of cytokines and chemokines (CHEMOtactic cytoKINES) in basal transmission and plasticity processes where signaling between peri-synaptic astrocytes, microglia and neurons plays an important role. Nevertheless, the exact mechanisms as to how cytokines, and in particular chemokines, participate in the molecular and cellular processes thought to subserve memory formation, plasticity processes and responsiveness to environmental stimuli remain to be clarified. Interestingly, in in vitro preparations, molecules like TNF-a, interleukin (IL)-1ß, IL-6, CX3CL1, CXCL12, CCL2 and CCL3 are implicated in synaptic formation and scaling, in modulation of glutamatergic transmission, in plasticity and neurogenesis, in particular in the hippocampus. The hippocampus is an extremely plastic structure, one of the main neurogenic niches in the adult brain, that exhibits a marked sensibility to environmental stimuli. Indeed exposure of mice to environmental enrichment (EE) modifies learning and memory abilities increasing neurogenesis and neuronal plasticity whether exposure to severe stressful experiences diminishes neurotrophic support, impairs neurogenesis, plasticity and cognition. In the hippocampus cytokines play a key role in mediating both positive as well as negative effects of the environment affecting neuronal plasticity also in stress related pathologies, such as depression. It has been reported that mice lacking type 1 receptor for IL-1 display impaired hippocampal memory and LTP that are restored by EE; moreover negative effects on neuronal plasticity (and thus behavior) induced by stress exposure can be prevented by blocking IL-1 activity. In addition, mice lacking IL-6 have improved cognitive functions whereas the absence of microglia-driven CX3CR1 signaling increases hippocampal plasticity and spatial memory occluding the potentiating effects of EE. However, the factors mediating the effect of environmental stimuli on behavior and plasticity has been only partially identified. Interestingly, it has been suggested that chemokines can play a key role in the flexibility of hippocampal structure and may modulate neuronal signaling during behavior. The question is how cytokines may translate environmental stimuli in plasticity and behavioral changes. This research topic is proposed to explore the role of cytokines, and more in particular chemokines, in the modulation of neuronal activity as a fundamental step for the correct brain wiring, function and susceptibility to environment. We encourage the submission of original research reports, review articles, commentaries, perspectives or short communications, in the following (but not limited to) topics:- Role of cytokines and chemokines in neuronal plasticity- Immune molecules and responsiveness to environment- Role of chemokine in the flexibility of hippocampal structure

All 3 Types of Glial Cells Are Important for Memory Formation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450251 Year: Pages: 150 DOI: 10.3389/978-2-88945-025-1 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2018-02-27 16:16:44
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The vertebrate brain contains neurons and 3 classical types of glia cells, astrocytes, oligodendrocytes and microglia. Astrocytes and microglia have mainly been studied in gray matter, whereas oligodendrocytes myelinate white matter tracts. Until recently microglial effects were considered mainly during pathological conditions, but is now known that microglia plays important roles also in normal brain function. All these 3 glial cell types and their collaboration with neurons are important for learning. The concept that glia cells are important for cognitive function is not new. A glial-neuronal theory of brain function was proposed by Galambos in 1961. Hyden and Egyhazi demonstrated glial RNA changes in microdissected glia cells during learning in rats in 1963, and astrocytic and oligodendrocytic involvement of K+-mediated effects of learning has been suggested and/or demonstrated from the 1960’s and onwards as recently reviewed by Hertz and Chen (Neuroscience and Biobehavioural Reviews, 2016). In 1969 van den Berg et al. showed compartmentation of glutamate in brain and thus of production of the neurotransmitters glutamate and GABA, which are essential for learning. That glutamate is synthesized in astrocytes because they in contrast to neurons express the enzyme pyruvate carboxylase was demonstrated 10-15 years later by Yu et al. in cultured astrocytes and Shank et al. in intact brain tissue. However, the present e-book focuses on more recent developments. Most information is available about astrocytic roles in learning. The importance of astrocytes in the tripartite synapse and of microglia in the tetrapartite synapse is illustrated in the front-page figure, which emphasizes the role of gliotransmitters and of Ca2+ transport through gap junctions, coupling astrocytes into a functional syncytium. Astrocytes are important for establishments of brain rhythms, which may differ in different cognitive tasks, and although the exact reason why knock-out of the astrocytic water channel AQP4 impairs memory remains to be established, several possibilities are discussed. The importance of the two astrocyte specific processes glutamate and glutamine formation and glycogenolysis is discussed in considerable detail. Glycogenolysis is important not only for astrocytic processes involved in learning, but also for those in neurons because glycolytically derived lactate has signaling functions in the extracellular space and may be accumulated in minute quantities into very specific and small neuronal structures. Some neurotransmitters stimulating glycogenolysis are also involved in psychiatric disease. Noradrenaline, released from locus coeruleus exerts direct effects on both astrocytes and neurons and in addition promotes secretion of corticotropin-releasing hormone and adrenocorticotrophic hormone (ACTH) in brain, and of glucocorticoids from the adrenal cortex, all of which are responsible for stress effects on learning. Lead causes memory impairment by inhibition of glutamine formation due to oxidative stress and reduced effectiveness of the glutathione system. The many adverse effects of fetal alcohol exposure on behaviour and learning are caused by a multitude of effects on all three types of glia cells. Traumatic brain injury also exerts multifactorial effects, including microglia/astrocyte-induced secretion of neuroinflammatory molecules and axonal disruption and oligodendrocytic dysfunction. In normal brain oligodendrocytes respond to the depolarization caused by neuronal activity with accelerated conduction velocity and increased compound action potentials which facilitate learning.

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