Готові списки джерел за темами / Neuron-glia interplay

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Добірка наукової літератури з теми "Neuron-glia interplay"

Автор: Grafiati

Опубліковано: 10 березня 2023

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Статті в журналах з теми "Neuron-glia interplay"

López-Bayghen, Esther, Sandra Rosas, Francisco Castelán, and Arturo Ortega. "Cerebellar Bergmann glia: an important model to study neuron–glia interactions." Neuron Glia Biology 3, no. 2 (May 2007): 155–67. http://dx.doi.org/10.1017/s1740925x0700066x.

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AbstractThe biochemical effects triggered by the action of glutamate, the main excitatory amino acid, on a specialized type of glia cells, Bergmann glial cells of the cerebellum, are a model system with which to study glia–neuronal interactions. Neuron to Bergmann glia signaling is involved in early stages of development, mainly in cell migration and synaptogenesis. Later, in adulthood, these cells have an important role in the maintenance and proper function of the synapses that they surround. Major molecular targets of this cellular interplay are glial glutamate receptors and transporters, both of which sense synaptic activity. Glutamate receptors trigger a complex network of signaling cascades that involve Ca2+ influx and lead to a differential gene-expression pattern. In contrast, Bergmann glia glutamate transporters participate in the removal of the neurotransmitter from the synaptic cleft and act also as signal transducers that regulate, in the short term, their own activity. These exciting findings strengthen the concept of active participation of glial cells in synaptic transmission and the involvement of neuron–glia circuits in the processing of brain information.

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Silva, Sandra L., Catarina Osório, Ana R. Vaz, Andreia Barateiro, Ana S. Falcão, Rui F. M. Silva, and Dora Brites. "Dynamics of neuron-glia interplay upon exposure to unconjugated bilirubin." Journal of Neurochemistry 117, no. 3 (March 23, 2011): 412–24. http://dx.doi.org/10.1111/j.1471-4159.2011.07200.x.

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Brancaccio, Marco. "Glia-neuron interplay drives circadian glycosphingolipid homeostasis and structural brain plasticity." Neuron 110, no. 19 (October 2022): 3058–60. http://dx.doi.org/10.1016/j.neuron.2022.08.024.

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Ureshino, Erustes, Bassani, Wachilewski, Guarache, Nascimento, Costa, Smaili, and Pereira. "The Interplay between Ca2+ Signaling Pathways and Neurodegeneration." International Journal of Molecular Sciences 20, no. 23 (November 28, 2019): 6004. http://dx.doi.org/10.3390/ijms20236004.

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Calcium (Ca2+) homeostasis is essential for cell maintenance since this ion participates in many physiological processes. For example, the spatial and temporal organization of Ca2+ signaling in the central nervous system is fundamental for neurotransmission, where local changes in cytosolic Ca2+ concentration are needed to transmit information from neuron to neuron, between neurons and glia, and even regulating local blood flow according to the required activity. However, under pathological conditions, Ca2+ homeostasis is altered, with increased cytoplasmic Ca2+ concentrations leading to the activation of proteases, lipases, and nucleases. This review aimed to highlight the role of Ca2+ signaling in neurodegenerative disease-related apoptosis, where the regulation of intracellular Ca2+ homeostasis depends on coordinated interactions between the endoplasmic reticulum, mitochondria, and lysosomes, as well as specific transport mechanisms. In neurodegenerative diseases, alterations-increased oxidative stress, energy metabolism alterations, and protein aggregation have been identified. The aggregation of α-synuclein, β-amyloid peptide (Aβ), and huntingtin all adversely affect Ca2+ homeostasis. Due to the mounting evidence for the relevance of Ca2+ signaling in neuroprotection, we would focus on the expression and function of Ca2+ signaling-related proteins, in terms of the effects on autophagy regulation and the onset and progression of neurodegenerative diseases.

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Lana, Daniele, Filippo Ugolini та Maria Grazia Giovannini. "Space-Dependent Glia–Neuron Interplay in the Hippocampus of Transgenic Models of β-Amyloid Deposition". International Journal of Molecular Sciences 21, № 24 (11 грудня 2020): 9441. http://dx.doi.org/10.3390/ijms21249441.

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This review is focused on the description and discussion of the alterations of astrocytes and microglia interplay in models of Alzheimer’s disease (AD). AD is an age-related neurodegenerative pathology with a slowly progressive and irreversible decline of cognitive functions. One of AD’s histopathological hallmarks is the deposition of amyloid beta (Aβ) plaques in the brain. Long regarded as a non-specific, mere consequence of AD pathology, activation of microglia and astrocytes is now considered a key factor in both initiation and progression of the disease, and suppression of astrogliosis exacerbates neuropathology. Reactive astrocytes and microglia overexpress many cytokines, chemokines, and signaling molecules that activate or damage neighboring cells and their mutual interplay can result in virtuous/vicious cycles which differ in different brain regions. Heterogeneity of glia, either between or within a particular brain region, is likely to be relevant in healthy conditions and disease processes. Differential crosstalk between astrocytes and microglia in CA1 and CA3 areas of the hippocampus can be responsible for the differential sensitivity of the two areas to insults. Understanding the spatial differences and roles of glia will allow us to assess how these interactions can influence the state and progression of the disease, and will be critical for identifying therapeutic strategies.

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Sugiura, Yoshie, and Weichun Lin. "Neuron–glia interactions: the roles of Schwann cells in neuromuscular synapse formation and function." Bioscience Reports 31, no. 5 (April 21, 2011): 295–302. http://dx.doi.org/10.1042/bsr20100107.

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The NMJ (neuromuscular junction) serves as the ultimate output of the motor neurons. The NMJ is composed of a presynaptic nerve terminal, a postsynaptic muscle and perisynaptic glial cells. Emerging evidence has also demonstrated an existence of perisynaptic fibroblast-like cells at the NMJ. In this review, we discuss the importance of Schwann cells, the glial component of the NMJ, in the formation and function of the NMJ. During development, Schwann cells are closely associated with presynaptic nerve terminals and are required for the maintenance of the developing NMJ. After the establishment of the NMJ, Schwann cells actively modulate synaptic activity. Schwann cells also play critical roles in regeneration of the NMJ after nerve injury. Thus, Schwann cells are indispensable for formation and function of the NMJ. Further examination of the interplay among Schwann cells, the nerve and the muscle will provide insights into a better understanding of mechanisms underlying neuromuscular synapse formation and function.

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ELMARIAH, SARINA B., ETHAN G. HUGHES, EUN JOO OH, and RITA J. BALICE-GORDON. "Neurotrophin signaling among neurons and glia during formation of tripartite synapses." Neuron Glia Biology 1, no. 4 (November 2004): 339–49. http://dx.doi.org/10.1017/s1740925x05000189.

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Synapse formation in the CNS is a complex process that involves the dynamic interplay of numerous signals exchanged between pre- and postsynaptic neurons as well as perisynaptic glia. Members of the neurotrophin family, which are widely expressed in the developing and mature CNS and are well-known for their roles in promoting neuronal survival and differentiation, have emerged as key synaptic modulators. However, the mechanisms by which neurotrophins modulate synapse formation and function are poorly understood. Here, we summarize our work on the role of neurotrophins in synaptogenesis in the CNS, in particular the role of these signaling molecules and their receptors, the Trks, in the development of excitatory and inhibitory hippocampal synapses. We discuss our results that demonstrate that postsynaptic TrkB signaling plays an important role in modulating the formation and maintenance of NMDA and GABAA receptor clusters at central synapses, and suggest that neurotrophin signaling coordinately modulates these receptors as part of mechanism that promotes the balance between excitation and inhibition in developing circuits. We also discuss our results that demonstrate that astrocytes promote the formation of GABAergic synapses in vitro by differentially regulating the development of inhibitory presynaptic terminals and postsynaptic GABAA receptor clusters, and suggest that glial modulation of inhibitory synaptogenesis is mediated by neurotrophin-dependent and -independent signaling. Together, these findings extend our understanding of how neuron–glia communication modulates synapse formation, maintenance and function, and set the stage for defining the cellular and molecular mechanisms by which neurotrophins and other cell–cell signals direct synaptogenesis in the developing brain.

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Wanke, Enzo, Francesca Gullo, Elena Dossi, Gaetano Valenza, and Andrea Becchetti. "Neuron-glia cross talk revealed in reverberating networks by simultaneous extracellular recording of spikes and astrocytes' glutamate transporter and K+ currents." Journal of Neurophysiology 116, no. 6 (December 1, 2016): 2706–19. http://dx.doi.org/10.1152/jn.00509.2016.

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Astrocytes uptake synaptically released glutamate with electrogenic transporters (GluT) and buffer the spike-dependent extracellular K+ excess with background K+ channels. We studied neuronal spikes and the slower astrocytic signals on reverberating neocortical cultures and organotypic slices from mouse brains. Spike trains and glial responses were simultaneously captured from individual sites of multielectrode arrays (MEA) by splitting the recorded traces into appropriate filters and reconstructing the original signal by deconvolution. GluT currents were identified by using dl-threo-β-benzyloxyaspartate (TBOA). K+ currents were blocked by 30 μM Ba2+, suggesting a major contribution of inwardly rectifying K+ currents. Both types of current were tightly correlated with the spike rate, and their astrocytic origin was tested in primary cultures by blocking glial proliferation with cytosine β-d-arabinofuranoside (AraC). The spike-related, time-locked inward and outward K+ currents in different regions of the astrocyte syncytium were consistent with the assumptions of the spatial K+ buffering model. In organotypic slices from ventral tegmental area and prefrontal cortex, the GluT current amplitudes exceeded those observed in primary cultures by several orders of magnitude, which allowed to directly measure transporter currents with a single electrode. Simultaneously measuring cell signals displaying widely different amplitudes and kinetics will help clarify the neuron-glia interplay and make it possible to follow the cross talk between different cell types in excitable as well as nonexcitable tissue.

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Panatier, Aude, Misa Arizono, and U. Valentin Nägerl. "Dissecting tripartite synapses with STED microscopy." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1654 (October 19, 2014): 20130597. http://dx.doi.org/10.1098/rstb.2013.0597.

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The concept of the tripartite synapse reflects the important role that astrocytic processes are thought to play in the function and regulation of neuronal synapses in the mammalian nervous system. However, many basic aspects regarding the dynamic interplay between pre- and postsynaptic neuronal structures and their astrocytic partners remain to be explored. A major experimental hurdle has been the small physical size of the relevant glial and synaptic structures, leaving them largely out of reach for conventional light microscopic approaches such as confocal and two-photon microscopy. Hence, most of what we know about the organization of the tripartite synapse is based on electron microscopy, which does not lend itself to investigating dynamic events and which cannot be carried out in parallel with functional assays. The development and application of superresolution microscopy for neuron–glia research is opening up exciting experimental opportunities in this regard. In this paper, we provide a basic explanation of the theory and operation of stimulated emission depletion (STED) microscopy, outlining the potential of this recent superresolution imaging modality for advancing our understanding of the morpho-functional interactions between astrocytes and neurons that regulate synaptic physiology.

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Kamal, Mohammad Amjad, Aziz Unnisa, and Nigel H. Greig. "Modeling the Interplay Between Neuron-Glia Cell Dysfunction and Glial Therapy in Autism Spectrum Disorder." Current Neuropharmacology 21 (December 21, 2022). http://dx.doi.org/10.2174/1570159x21666221221142743.

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Abstract: Autism spectrum disorder (ASD) is a complicated, interpersonally defined, static condition of the underdeveloped brain. Although the aetiology of autism remains unclear, disturbance of neuron-glia interactions has lately been proposed as a significant event in the pathophysiology of ASD. In recent years, the contribution of glial cells to autism has been overlooked. In addition to neurons, glial cells play an essential role in mental activities, and a new strategy that emphasises neuron-glia interactions should be applied. Disturbance of neuron-glia connections has lately been proposed as a significant event in the pathophysiology of ASD because aberrant neuronal network formation and dysfunctional neurotransmission are fundamental to the pathology of the condition. In ASD, neuron and glial cell number changes cause brain circuits to malfunction and impact behaviour. A study revealed that reactive glial cells result in the loss of synaptic functioning and induce autism under inflammatory conditions. Recent discoveries also suggest that dysfunction or changes in the ability of microglia to carry out physiological and defensive functions (such as failure in synaptic elimination or aberrant microglial activation) may be crucial for developing brain diseases, especially autism. The cerebellum, white matter, and cortical regions of autistic patients showed significant microglial activation. Reactive glial cells result in the loss of synaptic functioning and induce autism under inflammatory conditions. Replacement of defective glial cells (Cell-replacement treatment), glial progenitor cell-based therapy, and medication therapy (inhibition of microglia activation) are all utilised to treat glial dysfunction. This review discusses the role of glial cells in ASD and the various potential approaches to treating glial cell dysfunction.

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Більше джерел

Дисертації з теми "Neuron-glia interplay"

Ugolini, Filippo, Maria Grazia Giovannini, and Lana Daniele. "A study on different patterns of alteration of the neuron-glia interplay in experimental models of neurodegeneration." Doctoral thesis, 2020. http://hdl.handle.net/2158/1214966.

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BRONZUOLI, MARIA ROSANNA. "Glia-neuron interplay in health and disease: pharmacological evidence for this required teamwork." Doctoral thesis, 2016. http://hdl.handle.net/11573/933462.

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Glia is a cell population highly present in the central nervous system (CNS) with the purpose, among other functions, to support neurons. In fact, many of these cells are closely in contact with neurons, actively participating to homeostatic support and synaptic transmission. For instance, astrocytes are considered integral part of the tripartite synapse. By this way, recent discoveries made possible to change perspective regarding the neuro-centric view of chronic neurodegenerative disorders, expanding the horizon to new players involved in the physiological and/or pathologic processes that take place in CNS. Better understanding the contribution of non-neuronal cells to these processes will be crucial for the development of new therapeutic approaches to counteract neurodegeneration. Moving from these assumptions, my studies focused on evaluating the role of glial cells in inducing and triggering the inflammatory processes during neurodegeneration and, in particular, on the events that lead these cells to an activated state named reactive gliosis. Moreover, the consequences caused by these processes on neuronal survival, and in a macroscopic manner, on learning and memory, were evaluated. To achieve such goals, I worked with different preclinical models of AD, both in vitro and in vivo, attempting to recreate at best the pathological hallmarks of pathology. In addition, since the crucial role of glial cells in the maintenance of brain homeostasis and their close connection with neuronal functioning and survival, the action of different molecules on neuroinflammation, as well as on neuronal survival, were tested.

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