BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain

By Jeffrey A. M. Coull, S. Beggs, D. Boudreau, D. Boivin, M. Tsuda, Kazuhide Inoue, C. Gravel, Michael W. Salter, Y. Koninck. Nature, 2005

1,914 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/41e0372cae413598b9790788bb464f7771313c14

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In Cellular and Molecular Neuroscience

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Citations in the corpus

The role of glia in the spinal cord in neuropathic and inflammatory pain. (2015, background): “Current evidence indicated that downstream effects of the activation of microglial purinergic receptors are mediated by the release of BDNF via the phosphorylation of p38 MAPK; the administration of an inhibitor of the BDNF receptor, TrkB, prevents the behavioural changes observed following the admi”
Cation-chloride cotransporters and neuronal function. (2009, background): “This loss of inhibition appeared to be mediated via BDNF released from activated spinal microglia (Coull et al., 2005).”
Deconstructing the Neuropathic Pain Phenotype to Reveal Neural Mechanisms (2012, positive): “The inhibitory effect of GABA is further reduced as BDNF released from microglia after nerve injury alters the anion reversal potential in some dorsal horn neurons decreasing or even phase shifting GABA’s actions on these neurons (Coull et al., 2005; Prescott et al., 2006).”
Microglia: new roles for the synaptic stripper. (2013, positive): “…Inc. receptor glycine binding site by microglia (Hayashi et al., 2006), signaling by fractalkine and its receptor (Paolicelli et al., 2011; Rogers et al., 2011), modulation of Cl gradient in neurons through microglial BDNF release (Coull et al., 2005) and purinergic signaling (Tsuda et al., 2010).”
Debris clearance by microglia: an essential link between degeneration and regeneration (2008, background): “Recent data also indicate that microglial-derived BDNF is implicated in neuropathic pain by causing a shift in the neuronal anion gradient of spinal lamina I neurons, thus contributing to tactile allodynia (Coull et al., 2005).”
Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain (2013, background): “Further investigations aimed at understanding chemokine-cytokine networks that are operative in the signal transduction of the pain response will prove beneficial in designing novel therapeutic strategies to alleviate neuropathic pain, a significant factor in neurodegenerative diseases.”
Inhibitory synaptic plasticity: spike timing-dependence and putative network function (2013, background): “…2009), [e.g., through downregulation of a neuron-specific K+/Cl− co-transporter (KCC2)] is linked to pathologies such as chronic pain, schizophrenia, and epilepsy (Coull et al., 2003; Buzsáki et al., 2007; De Koninck, 2007; Kaila and Miles, 2010; Wamsteeker and Bains, 2010; Huberfeld et al., 2011).”
Depression as a microglial disease. (2015, background): “Microglial BDNF is an important mediator of microglia-to-neuron communication [195], particularly via local interactions between microglial processes and TRKB (neurotrophic tyrosine kinase receptor type 2) receptors on synaptic elements [177].”
Models and mechanisms of hyperalgesia and allodynia. (2009, background): “, due to a reversal of the anion gradient in the postsynaptic neuron (88, 89).”
p38 MAPK, microglial signaling, and neuropathic pain (2007, background): “Although brain-derived neurotrophic factor (BDNF) is not regarded as an IFM, it is produced by microglia and plays important role in neuropathic pain development [14].”