Synaptic scaling mediated by glial TNF-alpha.

By D. Stellwagen, R. Malenka. Nature, 2006

837 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/d77cfa89241b32c95dd2c21849709f04867e1b85

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Citations in the corpus

Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, unknown): “Astrocytes also mediate other forms of plasticity, such as homeostatic synaptic 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 th”
Sepsis: current dogma and new perspectives. (2014, background): “TNF has been directly implicated as a neuromodulatory factor that establishes synaptic scaling, the process by which neurons adapt to repetitive stimulation responses (Stellwagen and Malenka, 2006).”
The mystery and magic of glia: a perspective on their roles in health and disease. (2008, background): “TNFa even plays a role in controlling normal function and plasticity of neural circuits in vitro and in vivo (Stellwagen and Malenka, 2006; Kaneko et al., 2008).”
Long term potentiation depends on release of D-serine from astrocytes (2010, unknown): “11).”
Synaptic signaling by all-trans retinoic acid in homeostatic synaptic plasticity (2008, background): “1 and CaM Kinase II (middle; [Shepherd et al., 2006; Thiagarajan et al., 2002]) and induces TNFa secretion from glia cells (right; [Stellwagen and Malenka, 2006]).”
Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017, background): “Microglia also influence another type of synaptic plasticity known as synaptic scaling, which promotes even adjustments in the strength of all synapses on a neuron in response to prolonged changes in the cell’s electrical activity (81).”
Evidence for a cytokine model of cognitive function. (2009, background): “In particular, it was shown that during prolonged inactivity TNF shifts neurons towards more excitation and less inhibition (Stellwagen and Malenka, 2006) (see Fig.”
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).”
Cell biology of astrocyte-synapse interactions (2017, unknown): “TNF-a release is decreased by glutamate (Stellwagen and Malenka, 2006).”
Debris clearance by microglia: an essential link between degeneration and regeneration (2008, background): “Debris clearance by microglia: an essential link between degeneration and regeneration”
Arc/Arg3.1 mediates homeostatic synaptic scaling of AMPA receptors. (2006, background): “A recent report indicates that TNF-a, which is derived from glia, is required for homeostatic upregulation of AMPARs in neurons induced by chronic activity blockade, but not downregulation due to increased activity (Stellwagen and Malenka, 2006).”
The Self-Tuning Neuron: Synaptic Scaling of Excitatory Synapses (2008, unknown): “…and adjust its synaptic weights up or down to keep this activity close to some set-point value, network activity will remain stable in the face of correlation-based changes in synaptic strength or developmental changes in synaptic connectivity (Figure 1C) (Miller, 1996; Sullivan and de Sa, 2006).”
Frontiers in Synaptic Neuroscience Synaptic Neuroscience (unknown): “Perhaps the most surprising result of this sort in recent years was made by Stellwagen and Malenka (2006), when they showed that a soluble released factor, a molecule called tumor necrosis factor alpha (TNFα) was required for synaptic scaling.”
The role of inflammation in the development of epilepsy (2018, background): “Glial cells sense extracellular glutamate levels and, upon detection of low levels of glutamate, release TNF-α to upregulate synapses and maintain a certain level of neuronal excitatory input [22].”
Hebbian and Homeostatic Plasticity Mechanisms in Regular Spiking and Intrinsic Bursting Cells of Cortical Layer 5 (2015, unknown): “In the visual cortex, this form of homeostatic plasticity is due to synaptic scaling and depends on TNFa both in vitro (Stellwagen and Malenka, 2006) and in vivo (Kaneko et al.”