Control of Synaptic Strength by Glial TNFα

By E. Beattie, D. Stellwagen, W. Morishita, J. Bresnahan, Byeong Keun Ha, M. von Zastrow, M. Beattie, R. Malenka. Science, 2002

1,120 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/63230e68e41eb2349b3b63378050ed598ea5e919

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

In Molecular Biology

In Neurology

Citations in the corpus

Regulation of synaptic connectivity by glia (2010, background): “Conversely, blocking TNF-α-mediated signalling was found to have the opposite effec”
Homeostatic synaptic plasticity: local and global mechanisms for stabilizing neuronal function. (2012, background): “…activity blockade, acute application of TNFa (or conditioned media from activity-blocked cultures) increases mEPSC amplitude, and scaling up in response to prolonged activity blockade is prevented by blocking TNFa signaling (Beattie et al. 2002; Stellwagen et al. 2005; Stellwagen and Malenka 2006).”
Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, background): “…scaling following prolonged inhibition of neuronal activity, via secretion of the pro-inflammatory cytokine TNFa (Kaneko et al., 2008; Stellwagen and Malenka, 2006), a known synaptic strength enhancer, which increases the surface expression of AMPA glutamatergic receptors (Beattie et al., 2002).”
Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis (2014, neutral): “It is likely NF-kB might regulate important aspects of astrocyte function that are needed to support MNs under insult in ALS, which may explain why no benefit was observed with astroglial NF-kB inhibition in SOD1-G93A mice (Beattie et al., 2002; Bracchi-Ricard et al., 2008).”
Conditional Knock-Out of Kir4.1 Leads to Glial Membrane Depolarization, Inhibition of Potassium and Glutamate Uptake, and Enhanced Short-Term Synaptic Potentiation (2007, background): “…neuronal excitability (Zhang et al., 2003; Tian et al., 2005), excitatory and inhibitory synaptic transmission and plasticity (Kang et al., 1998; Beattie et al., 2002; Yang et al., 2003; Fiacco and McCarthy, 2004; Pascual et al., 2005), as well as synaptogenesis and neuronal wiring…”
Astrocytes Control Synapse Formation, Function, and Elimination (2015, positive): “Astrocytederived TNF-a rapidly induces the surface insertion of GluA1-containing AMPARs (within 15 min of treatment), causing an increase in the frequency but not amplitude of mEPSCs in cultured hippocampal neurons (Beattie et al. 2002).”
Homeostatic control of neural activity: from phenomenology to molecular design. (2006, background): “In the vertebrate CNS, there is evidence that quantal scaling can be influenced by both BDNF and glial-derived TNF-alpha (Desai et al. 1999a, Leslie et al. 2001, Beattie et al. 2002).”
The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “In hippocampal neurons TNF, via a TNFR1-PI3K signalling pathway, has been shown to promote excitability through increases in AMPA receptor expression (Beattie et al., 2002), and decreases in GABAA receptors (Stellwagen et al., 2005).”
Sulforhodamine 101 as a specific marker of astroglia in the neocortex in vivo (2004, background): “A multitude of signaling tasks is proposed for astroglia, including the modulation of synaptic functio”
The Self-Tuning Neuron: Synaptic Scaling of Excitatory Synapses (2008, background): “Application of TNFα to hippocampal or cortical cultures rapidly (within 15 min) increases mEPSC amplitude and surface number of AMPA receptors (Beattie et al., 2002; Stellwagen et al., 2005; Stellwagen and Malenka, 2006).”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “Specifically, secretion of the proinflammatory cytokine tumor necrosis factor-a from glial cells appears to be necessary for the increase in the level of synaptic AMPARs caused by extended periods of activity blockade (Beattie et al, 2002; Stellwagen et al, 2005; Stellwagen and Malenka, 2006).”
Too many cooks? Intrinsic and synaptic homeostatic mechanisms in cortical circuit refinement. (2011, background): “…for example, Arc interacts with the endocytic machinery that removes AMPAR from the membrane (Chowdhury et al. 2006), TNFα directly increases synaptic AMPAR accumulation (Beattie et al. 2002; Stellwagen et al. 2005), and Beta3 integrins regulate AMPAR surface expression (Cingolani et al. 2008).”
Astrocytes, from brain glue to communication elements: the revolution continues (2005, background): “The strength of the same synapses is under the tonic control of astrocyte-released TNF&alpha”