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Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation
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 syna...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976900/ https://www.ncbi.nlm.nih.gov/pubmed/29861718 http://dx.doi.org/10.1155/2018/8430123 |
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author | Rizzo, Francesca Romana Musella, Alessandra De Vito, Francesca Fresegna, Diego Bullitta, Silvia Vanni, Valentina Guadalupi, Livia Stampanoni Bassi, Mario Buttari, Fabio Mandolesi, Georgia Centonze, Diego Gentile, Antonietta |
author_facet | Rizzo, Francesca Romana Musella, Alessandra De Vito, Francesca Fresegna, Diego Bullitta, Silvia Vanni, Valentina Guadalupi, Livia Stampanoni Bassi, Mario Buttari, Fabio Mandolesi, Georgia Centonze, Diego Gentile, Antonietta |
author_sort | Rizzo, Francesca Romana |
collection | PubMed |
description | 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-1β (IL-1β) 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-β 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-1β 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. |
format | Online Article Text |
id | pubmed-5976900 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-59769002018-06-03 Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation Rizzo, Francesca Romana Musella, Alessandra De Vito, Francesca Fresegna, Diego Bullitta, Silvia Vanni, Valentina Guadalupi, Livia Stampanoni Bassi, Mario Buttari, Fabio Mandolesi, Georgia Centonze, Diego Gentile, Antonietta Neural Plast Review Article 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-1β (IL-1β) 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-β 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-1β 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. Hindawi 2018-05-14 /pmc/articles/PMC5976900/ /pubmed/29861718 http://dx.doi.org/10.1155/2018/8430123 Text en Copyright © 2018 Francesca Romana Rizzo et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Rizzo, Francesca Romana Musella, Alessandra De Vito, Francesca Fresegna, Diego Bullitta, Silvia Vanni, Valentina Guadalupi, Livia Stampanoni Bassi, Mario Buttari, Fabio Mandolesi, Georgia Centonze, Diego Gentile, Antonietta Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation |
title | Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation |
title_full | Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation |
title_fullStr | Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation |
title_full_unstemmed | Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation |
title_short | Tumor Necrosis Factor and Interleukin-1β Modulate Synaptic Plasticity during Neuroinflammation |
title_sort | tumor necrosis factor and interleukin-1β modulate synaptic plasticity during neuroinflammation |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5976900/ https://www.ncbi.nlm.nih.gov/pubmed/29861718 http://dx.doi.org/10.1155/2018/8430123 |
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