ArticleThe Journal of clinical investigation2016
Cortical astrocytes rewire somatosensory cortical circuits for peripheral neuropathic pain.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 203 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Developmental changes in CaScientific reports · 2026Article
- Article
- Astrocyte store-operated calcium entry is required for centrally mediated neuropathic pain.Pain reports · 2026Article
- Spinal Cord Stimulation Alleviates Neuropathic Pain Involves Regulation of the CaCellular and molecular neurobiology · 2026Article
- Altered astrocyte-neuron crosstalk in progressive supranuclear palsy: integrated evidence from proteomics and magnetic resonance spectroscopy.Acta neuropathologica · 2026Article
- Sphingosine-1-Phosphate Receptor 1 regulates competition dependent astrocyte morphogenesis and tiling in murine cortex.bioRxiv : the preprint server for biology · 2026Article
- Astrocyte CaBiomolecules · 2026Review
- Caudal Granular Insular Cortex to Somatosensory Cortex I: A Critical Pathway for the Transition of Acute to Chronic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Astrocytic PERK Deficiency Drives Prefrontal Circuit Dysfunction and Depressive-Like Behaviors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Increased Activity of CaV3.2 Channels Contributes to Nociceptors' Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Celastrol Ameliorates Vincristine-induced Neuropathic Pain by Inhibiting Spinal Astrocyte Hyperactivation-mediated Inflammation, Oxidative Stress, and Apoptosis.Current neuropharmacology · 2026Article
- A 3D-1D-0D multiscale model of the neuro-glial-vascular unit for synaptic and vascular dynamics in the dorsal vagal complex.Journal of mathematical biology · 2025Article
- Article
- Sensory abnormalities in autism spectrum disorder and their in vitro modeling.Translational psychiatry · 2025Review
- Role of astrocytes in diabetic neuropathy: Review of their involvement in disease mechanisms.World journal of diabetes · 2025Review
- Recent Insights on Supraspinal Astrocytes in Chronic Pain.Neurochemical research · 2025Review
- Review
- Review
- Optogenetic activation of cortical microglia promotes neuronal activity and pain hypersensitivity.Cell reports · 2025Article
57 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-term treatments to ameliorate peripheral neuropathic pain that includes mechanical allodynia are limited. While glial activation and altered nociceptive transmission within the spinal cord are associated with the pathogenesis of mechanical allodynia, changes in cortical circuits also accompany peripheral nerve injury and may represent additional therapeutic targets. Dendritic spine plasticity in the S1 cortex appears within days following nerve injury; however, the underlying cellular mechanisms of this plasticity and whether it has a causal relationship to allodynia remain unsolved. Furthermore, it is not known whether glial activation occurs within the S1 cortex following injury or whether it contributes to this S1 synaptic plasticity. Using in vivo 2-photon imaging with genetic and pharmacological manipulations of murine models, we have shown that sciatic nerve ligation induces a re-emergence of immature metabotropic glutamate receptor 5 (mGluR5) signaling in S1 astroglia, which elicits spontaneous somatic Ca2+ transients, synaptogenic thrombospondin 1 (TSP-1) release, and synapse formation. This S1 astrocyte reactivation was evident only during the first week after injury and correlated with the temporal changes in S1 extracellular glutamate levels and dendritic spine turnover. Blocking the astrocytic mGluR5-signaling pathway suppressed mechanical allodynia, while activating this pathway in the absence of any peripheral injury induced long-lasting (>1 month) allodynia. We conclude that reawakened astrocytes are a key trigger for S1 circuit rewiring and that this contributes to neuropathic mechanical allodynia.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.