Control of synaptic strength by glial TNFalpha.

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

665 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/6fe0d035199f3d88a99d5cf6dfd5d153b62cca0d

How researchers see this paper

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

1. Gina G. Turrigiano
2. Taro Toyoizumi
3. J. Burda
4. A. Citri
5. Megumi Kaneko
6. M. Sofroniew
7. G. Davis
8. R. Malenka

Citations in the corpus

• Synaptic signaling by all-trans retinoic acid in homeostatic synaptic plasticity (2008, background): “In addition to these neuron/muscle-autonomous factors, gliaderived factors such as the cytokine TNFa were demonstrated to control synaptic strength and to influence homeostatic synaptic plasticity (Beattie et al., 2002; Stellwagen and Malenka, 2006).”
• 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).”
• Astrocyte roles in traumatic brain injury (2015, background): “…of homeostatic synaptic plasticity, tunes global excitatory synaptic strength to fluctuations in firing rate by increasing postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) density across all of a neurons’ synapses (Turrigiano et al., 1998; Beattie et al., 2002).”
• Microglia induce motor neuron death via the classical NF-κB pathway in amyotrophic lateral sclerosis (2014, unknown): “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).”
• Cell biology of astrocyte-synapse interactions (2017, unknown): “…levels at existing synapses and conversely decreases GABAA receptors at inhibitory synapses, leading to overall increased neuronal activity, and is involved in homeostatic scaling to maintain neuronal network activity (Beattie et al., 2002; Stellwagen et al., 2005; Stellwagen and Malenka, 2006).”
• Modeling the dynamic interaction of Hebbian and homeostatic plasticity. (2014, background): “The oscillations arise because when y reaches y0, q still reflects the earlier weight values, soweight change continues in the same direction until q catches up.”
• Microglia activation triggers astrocyte-mediated modulation of excitatory neurotransmission (2011, background): “Glial TNF-α has been shown to rapidly increase EPSC frequency at AMPAergic synapses with no associated change in amplitude (33) and be necessary for astrocytic modulation of neuronal activity (36).”
• Physiology of Astroglia. (2018, unknown): “TNFMediates AMPA (117) and GABA receptor trafficking (1408); affects and may even induce synaptic plasticity; impairs learning and memory (621).”
• Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, unknown): “…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).”
• Cytokines and CNS development. (2009, unknown): “Exogenous TNFa modulates synaptic strength in hippocampal neurons by rapidly promoting surface expression of AMPA-type glutamate receptors (AMPAR), and interfering with TNFa signaling using TNFa antibodies or a soluble form of the TNFR1 (sTNFR1) decreases AMPAR surface expression (Beattie et al., 20”
• Brain Inflammation in Epilepsy: Experimental and Clinical Evidence (2005, background): “Conversely, TNF-α causes endocytosis of GABAA receptors, thus resulting in decreased inhibitory strength (27,82).”
• The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, unknown): “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).”
• 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).”
• Glia and pain: Is chronic pain a gliopathy? (2013, background): “TNF-a is known to induce the trafficking and surface expression of AMPA receptors in hippocampal neurons [12,220].”
• 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).”