Tumor Necrosis Factor and Interleukin-1<i>β</i> Modulate Synaptic Plasticity during Neuroinflammation
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- Francesca Romana Rizzo
- Synaptic Immunopathology Lab, Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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- Alessandra Musella
- Synaptic Immunopathology Lab, IRCCS San Raffaele, Via di Val Cannuta 247, 00166 Rome, Italy
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- Francesca De Vito
- Synaptic Immunopathology Lab, Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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- Diego Fresegna
- Synaptic Immunopathology Lab, Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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- Silvia Bullitta
- Synaptic Immunopathology Lab, Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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- Valentina Vanni
- Synaptic Immunopathology Lab, Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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- Livia Guadalupi
- Synaptic Immunopathology Lab, IRCCS San Raffaele, Via di Val Cannuta 247, 00166 Rome, Italy
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- Mario Stampanoni Bassi
- Unit of Neurology and Unit of Neurorehabilitation, IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, 86077 Pozzilli, Italy
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- Fabio Buttari
- Unit of Neurology and Unit of Neurorehabilitation, IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, 86077 Pozzilli, Italy
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- Georgia Mandolesi
- Synaptic Immunopathology Lab, IRCCS San Raffaele, Via di Val Cannuta 247, 00166 Rome, Italy
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- Diego Centonze
- Synaptic Immunopathology Lab, Department of Systems Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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- Antonietta Gentile
- Unit of Neurology and Unit of Neurorehabilitation, IRCCS Istituto Neurologico Mediterraneo (INM) Neuromed, 86077 Pozzilli, Italy
Abstract
<jats:p>Cytokines are constitutively released in the healthy brain by resident myeloid cells to keep proper synaptic plasticity, either in the form of Hebbian synaptic plasticity or of homeostatic plasticity. However, when cytokines dramatically increase, establishing a status of neuroinflammation, the synaptic action of such molecules remarkably interferes with brain circuits of learning and cognition and contributes to excitotoxicity and neurodegeneration. Among others, interleukin-1<jats:italic>β</jats:italic> (IL-1<jats:italic>β</jats:italic>) and tumor necrosis factor (TNF) are the best studied proinflammatory cytokines in both physiological and pathological conditions and have been invariably associated with long-term potentiation (LTP) (Hebbian synaptic plasticity) and synaptic scaling (homeostatic plasticity), respectively. Multiple sclerosis (MS) is the prototypical neuroinflammatory disease, in which inflammation triggers excitotoxic mechanisms contributing to neurodegeneration. IL-<jats:italic>β</jats:italic> and TNF are increased in the brain of MS patients and contribute to induce the changes in synaptic plasticity occurring in MS patients and its animal model, the experimental autoimmune encephalomyelitis (EAE). This review will introduce and discuss current evidence of the role of IL-1<jats:italic>β</jats:italic> and TNF in the regulation of synaptic strength at both physiological and pathological levels, in particular speculating on their involvement in the synaptic plasticity changes observed in the EAE brain.</jats:p>
Journal
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- Neural Plasticity
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Neural Plasticity 2018 1-12, 2018
Hindawi Limited
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Details 詳細情報について
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- CRID
- 1360294647846866048
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- ISSN
- 16875443
- 20905904
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- Data Source
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- Crossref