Cytokines and brain excitability.
TLDR
Findings from both the clinical literature and from in vivo and in vitro laboratory studies suggest that cytokines can increase seizure susceptibility and may be involved in epileptogenesis.About:
This article is published in Frontiers in Neuroendocrinology.The article was published on 2012-01-01 and is currently open access. It has received 319 citations till now. The article focuses on the topics: Microglia & Epileptogenesis.read more
Citations
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The role of inflammation in epilepsy
TL;DR: This work focuses on the rapidly growing body of evidence that supports the involvement of inflammatory mediators—released by brain cells and peripheral immune cells—in both the origin of individual seizures and the epileptogenic process.
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Glia and epilepsy: excitability and inflammation
TL;DR: This review critically evaluates the role of glia-induced hyperexcitability and inflammation in epilepsy and points to a significant contribution by non-neuronal cells, the glia--especially astrocytes and microglia--in the pathophysiology of epilepsy.
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Janus-faced microglia: beneficial and detrimental consequences of microglial phagocytosis
TL;DR: The present review will summarize the current state of the literature regarding the role of microglial phagocytosis in maintaining tissue homeostasis in health as in disease.
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Neuromodulatory properties of inflammatory cytokines and their impact on neuronal excitability.
TL;DR: Evidence that dysregulation of their biosynthesis and cellular release, or alterations in receptor-mediated intracellular pathways in target cells, leads to neuronal cell dysfunction and modifications in neuronal network excitability is reported.
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Neuroinflammatory pathways as treatment targets and biomarkers in epilepsy.
TL;DR: Understanding is focused on the IL-1 receptor–Toll-like receptor 4 axis, the arachidonic acid–prostaglandin cascade, oxidative stress and transforming growth factor-β signalling associated with blood–brain barrier dysfunction, all of which are pathways that are activated in pharmacoresistant epilepsy in humans and that can be modulated in animal models to produce therapeutic effects on seizures.
References
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Activity-dependent scaling of quantal amplitude in neocortical neurons
TL;DR: A new form of synaptic plasticity is described that increases or decreases the strength of all of a neuron's synaptic inputs as a function of activity, and may help to ensure that firing rates do not become saturated during developmental changes in the number and strength of synaptic inputs.
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Systemic LPS Causes Chronic Neuroinflammation and Progressive Neurodegeneration
Liya Qin,Xuefei Wu,Michelle L. Block,Yuxin Liu,Yuxin Liu,George R. Breese,Jau-Shyong Hong,Darin J. Knapp,Fulton T. Crews +8 more
TL;DR: It is demonstrated that through TNFα, peripheral inflammation in adult animals can activate brain microglia to produce chronically elevated pro‐inflammatory factors and induce delayed and progressive loss of DA neurons in the SN, providing valuable insight into the potential pathogenesis and self‐propelling nature of Parkinson's disease.
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Synaptic scaling mediated by glial TNF-α
TL;DR: This work shows that synaptic scaling in response to prolonged blockade of activity is mediated by the pro-inflammatory cytokine tumour-necrosis factor-α (TNF-α), and suggests that by modulating TNF- α levels, glia actively participate in the homeostatic activity-dependent regulation of synaptic connectivity.
Journal ArticleDOI
The role of inflammation in epilepsy
TL;DR: This work focuses on the rapidly growing body of evidence that supports the involvement of inflammatory mediators—released by brain cells and peripheral immune cells—in both the origin of individual seizures and the epileptogenic process.
Journal ArticleDOI
Control of Synaptic Strength by Glial TNFα
Eric C. Beattie,David Stellwagen,Wade Morishita,Jacqueline C. Bresnahan,Byeong Keun Ha,Mark von Zastrow,Michael S. Beattie,Robert C. Malenka +7 more
TL;DR: It is shown that a protein produced by glia, tumor necrosis factor α (TNFα), enhances synaptic efficacy by increasing surface expression of AMPA receptors, which may play roles in synaptic plasticity and modulating responses to neural injury.