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Dual role of microglia in health and disease: pushing the balance towards repair

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194926 Year: Pages: 101 DOI: 10.3389/978-2-88919-492-6 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2015-11-16 15:44:59
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Microglial cells play a vital role in the innate immune response occurring in the Central Nervous System (CNS). Under physiologic conditions, microglia dynamically patrol the brain parenchyma and participate in the remodeling of active neuronal circuits. Accordingly, microglia can boost synaptic plasticity by removing apoptotic cells and by phagocytizing axon terminals and dendritic spines that form inappropriate neural connections. Upon brain and spinal cord injury or infection, microglia act as the first line of immune defense by promoting the clearance of damaged cells or infectious agents and by releasing neurotrophins and/ or proneurogenic factors that support neuronal survival and regeneration.Recently, two main pathways were suggested for microglia activation upon stimuli. Classical activation is induced by Toll-like receptor agonists and Th1 cytokines and polarizes cells to an M1 state, mainly leading to the release of TNF-alpha, IL-6 and nitric oxide and to grave neural damage. Alternative activation is mediated by Th2 cytokines and polarizes cells to an M2a state inducing the release of antiinflammatory factors. These findings have further fueled the discussion on whether microglia has a detrimental or beneficial action (M1 or M2-associated phenotypes, respectively) in the diseased or injured CNS and, more importantly, on whether we can shift the balance to a positive outcome.Although microglia and macrophages share several common features, upon M1 and M2 polarizing conditions, they are believed to develop distinct phenotypic and functional properties which translate into different patterns of activity. Moreover, microglia/macrophages seem to have developed a tightly organized system of maintenance of CNS homeostasis, since cells found in different structures have different morphology and specific function (e.g. meningeal macrophages, perivascular macrophages, choroid plexus macrophages). Nevertheless, though substantial work has been devoted to microglia function, consensus around their exact origin, their role during development, as well as the exact nature of their interaction with other cells of the CNS has not been met.This issue discusses how microglial cells sustain neuronal activity and plasticity in the healthy CNS as well as the cellular and molecular mechanisms developed by microglia in response to injury and disease. Understanding the mechanisms involved in microglia actions will enforce the development of new strategies to promote an efficient CNS repair by committing microglia towards neuronal survival and regeneration.

Neuronal and glial structural plasticity induced by drugs of abuse

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889195985 Year: Pages: 90 DOI: 10.3389/978-2-88919-598-5 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Therapeutics
Added to DOAB on : 2016-03-10 08:14:32
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Drugs of abuse induce a host of alterations in brain structure and function, ranging from changes in gene expression and epigenetic processes to aberrant synaptic plasticity to volumetric changes in discrete brain regions. These alterations can be drug class-specific, and are not confined to neurons, as drugs of abuse also induce molecular and cellular alterations in various glial cell types such as astrocytes and microglia. The phenomenon of drug-induced plasticity includes changes in dendritic branching and architecture, dendritic spine density and morphology, astrocyte-neuronal interactions, dysregulation of glutamatergic and GABAergic signaling, and alterations in myelination or microglial phenotype. This drug-induced "rewiring" of the brain at numerous levels can contribute to the development, maintenance, and persistence of the addicted state, as well as associated deficits in normal cognitive functioning. The aim of this Research Topic is to collect recent and important findings related to the structural alterations produced by drug of abuse in neurons, glial, and other cell types of the central nervous system.

Keywords

plasticity --- Dendrite --- Spine --- Glutamate --- Dopamine --- GABA --- Neuron --- glia --- astrocyte --- Addiction

Cellular and molecular mechanisms of motor neuron death in amyotrophic lateral sclerosis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193769 Year: Pages: 190 DOI: 10.3389/978-2-88919-376-9 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2015-11-19 16:29:12
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Amyotrophic lateral sclerosis (ALS), which was described since 1869 by Jean Martin Charcot, is a devastating neurodegenerative disease characterized by the selective and progressive loss of upper and lower motor neurons of the cerebral cortex, brainstem and the spinal cord. The cognitive process is not affected and is not merely the result of aging because may occur at young ages. The only known cause of the disease is associated with genetic mutations, mainly in the gene encoding superoxide dismutase 1 (familial ALS), whereas there is no known cause of the sporadic form of ALS (SALS), which comprises >90% of cases. Both ALS types develop similar histopathological and clinical characteristics, and there is no treatment or prevention of the disease. Because effective treatments for ALS, as for other neurodegenerative diseases, can only result from the knowledge of their cellular and molecular pathophysiological mechanisms, research on such mechanisms is essential. Although progress in neurochemical, physiological and clinical investigations in the last decades has identified several mechanisms that seem to be involved in the cell death process, such as glutamate-mediated excitotoxicity, alterations of inhibitory circuits, inflammatory events, axonal transport deficits, oxidative stress, mitochondrial dysfunction and energy failure, the understanding of the origin and temporal progress of the disease is still incomplete and insufficient. Clearly, there is a need of further experimental models and approaches to discern the importance of such mechanisms and to discover the factors that determine the selective death of motor neurons characteristic of ALS, in contrast to other neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease. Whereas studies in vitro in cell cultures, tissue slices or organotypic preparations can give useful information regarding cellular and molecular mechanisms, the experiments in living animal models obviously reflect more closely the situation in the human disease, provided that the symptoms and their development during time mimics as close as possible those of the human disease. It is necessary to correlate the experimental findings in vitro with those in vivo, as well as those obtained in genetic models with those in non-genetic models, aiming at designing and testing therapeutic strategies based on the results obtained.

Transcellular Cycles Underlying Neurotransmission

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196548 Year: Pages: 105 DOI: 10.3389/978-2-88919-654-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-08-16 10:34:25
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Synaptic transmission demands the operation of a highly specialized metabolic machinery involving the transfer of metabolites and neurotransmitters between neurons, astrocytes and microvessels. In the last years, important advances have occurred in our understanding of the mechanisms underlying cerebral activation, neuroglial coupling and the associated neurovascular response. Briefly, exacerbated oxygen consumption in stimulated neurons is thought to trigger glycolytic lactate and glucose transfer from astrocytes which, in turn, obtain these fuels from the microvasculature. Neurotransmitter release is made possible by a combination of transcellular cycles exchanging metabolites between these three compartments, returning eventually the synapsis to its pre-firing situation in the resting periods. In spite of the enormous progresses achieved in recent years, the drivers determining the predominant direction of the fluxes, their quantitative contribution and their energy requirements, have remained until today incompletely understood, more particularly under the circumstances prevailing in vivo. In many instances, progress derived from the implementation of novel methodological approaches including advanced neuroimaging and neurospectroscopy methods. As a consequence, literature in the field became vast, diverse and spread within journals of different specialities. The e-book "Transcellular cycles underlying neurotransmission" aims to summaryze in a single volume, recent progress achieved in hypothesis, methods and interpretations on the trafficking of metabolites between neurons and glial cells, and the associated mechanisms of neurovascular coupling.

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