Spatial and temporal activation of spinal glial cells: Role of gliopathy in central neuropathic pain following spinal cord injury in rats
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TLDR
Time and regional dependence of glial activation and activation mechanisms in various SCI models in rats are described and demonstrated that dysfunctional glia, a condition called "gliopathy", is a key contributor in the underlying cellular mechanisms contributing to neuropathic pain.About:
This article is published in Experimental Neurology.The article was published on 2012-04-01 and is currently open access. It has received 238 citations till now. The article focuses on the topics: Gliosis & Neuron.read more
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Journal ArticleDOI
Glia and pain: Is chronic pain a gliopathy?
Ru-Rong Ji,Temugin Berta +1 more
TL;DR: Chronic pain could be a result of "gliopathy," that is, dysregulation of glial functions in the central and peripheral nervous system, and an update on recent advances is provided and remaining questions are discussed.
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In vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer's disease model.
TL;DR: It is shown that reactive glial cells in the cortex of stab-injured or Alzheimer's disease model mice can be directly reprogrammed into functional neurons in vivo using retroviral expression of a single neural transcription factor, NeuroD1.
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Microglia in Pain: Detrimental and Protective Roles in Pathogenesis and Resolution of Pain.
TL;DR: It is highlighted that microglial mediators such as pro- and anti-inflammatory cytokines are powerful neuromodulators that regulate synaptic transmission and pain via neuron-glial interactions and revealed an emerging role of microglia in the resolution of pain, in part via specialized pro-resolving mediators including resolvins, protectins, and maresins.
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Astrocytes in chronic pain and itch
TL;DR: The cellular and molecular mechanisms through which astrocytes contribute to the induction and maintenance of chronic pain and itch are described and targeting the specific pathways that are responsible for astrogliopathy is suggested.
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Human Stem Cell-Derived Spinal Cord Astrocytes with Defined Mature or Reactive Phenotypes
Laurent Roybon,Nuno Jorge Lamas,Alejandro Garcia-Diaz,Eun Ju Yang,Rita Sattler,Vernice Jackson-Lewis,Yoon A. Kim,C. Alan Kachel,Jeffrey D. Rothstein,Serge Przedborski,Hynek Wichterle,Christopher E. Henderson +11 more
TL;DR: Using early neuralization, spinal cord astrocytes are generated from mouse or human embryonic or induced pluripotent stem cells with high efficiency and short exposure to fibroblast growth factor 1 (FGF1) or FGF2 was sufficient to direct these astroCytes selectively toward a mature quiescent phenotype, as judged by both marker expression and functional analysis.
References
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BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain
Jeffrey A. M. Coull,Simon Beggs,Dominic Boudreau,Dominick Boivin,Makoto Tsuda,Kazuhide Inoue,Claude Gravel,Michael W. Salter,Yves De Koninck +8 more
TL;DR: It is shown that ATP-stimulated microglia cause a depolarizing shift in the anion reversal potential (Eanion) in spinal lamina I neurons, and that BDNF is a crucial signalling molecule betweenmicroglia and neurons.
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The neuropathic pain triad: neurons, immune cells and glia
Joachim Scholz,Clifford J. Woolf +1 more
TL;DR: Immunosuppression and blockade of the reciprocal signaling pathways between neuronal and non-neuronal cells offer new opportunities for disease modification and more successful management of pain.
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Direct signaling from astrocytes to neurons in cultures of mammalian brain cells
TL;DR: Astrocytes are shown to directly modulate the free cytosolic calcium, and hence transmission characteristics, of neighboring neurons, which suggests that the astrocytic-neuronal signaling is mediated through intercellular connections rather than synaptically.
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CXCR4-activated astrocyte glutamate release via TNFalpha: amplification by microglia triggers neurotoxicity.
Paola Bezzi,Maria Domercq,Liliana Brambilla,Rossella Galli,Dominique Schols,Erik De Clercq,Angelo L. Vescovi,Giacinto Bagetta,George Kollias,Jacopo Meldolesi,Andrea Volterra +10 more
TL;DR: It is demonstrated that altered glial communication has direct neuropathological consequences and that agents interfering with CXCR4-dependent astrocyte–microglia signaling prevent neuronal apoptosis induced by the HIV-1 coat glycoprotein, gp120IIIB.
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Broad expression of Toll-like receptors in the human central nervous system
TL;DR: Broad and regulated expression of Toll-like receptors both in vitro and in vivo by human glia cells is revealed.
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