ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.
What it found
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Who cites it
133 citing papers in PubMed, 244 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Neuropathic pain in traumatic brain injury: consequences, mechanisms, and therapeutic avenues.Inflammopharmacology · 2026Review
- Article
- Neurophysiological Basis of Short-Chain Fatty Acid Action in Pain Modulation: Therapeutic Implications.International journal of molecular sciences · 2025Review
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large-Caliber Fibers in Mice.Journal of neurochemistry · 2025Article
- A Short-Chain Fatty Acid, Butyrate, Suppresses the Hyperexcitability of Rat Nociceptive Primary Neurons Involved in Inflammatory Hyperalgesia.Molecules (Basel, Switzerland) · 2025Article
- C5a in the peripheral plasma of female fibromyalgia patients is elevated but not related to pain sensitivity as in healthy controls.Scientific reports · 2025Article
- Targeting C1q prevents microglia-mediated synaptic removal in neuropathic pain.Nature communications · 2025Article
- Reducing IgG accumulation via neonatal Fc receptor (FcRn) blockade relieves neuropathic pain.Brain, behavior, and immunity · 2025Article
- The complement system in human pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- Gene therapy for chronic pain management.Cell reports. Medicine · 2024Review
- The complement system: a potential target for the comorbidity of chronic pain and depression.The Korean journal of pain · 2024Article
- The complement system in neurodegenerative and inflammatory diseases of the central nervous system.Frontiers in neurology · 2024Review
- Complement Receptor C3aR1 Contributes to Paclitaxel-Induced Peripheral Neuropathic Pain in Mice and Rats.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Cold exposure induces vaso-occlusion and pain in sickle mice that depend on complement activation.Blood · 2023Article
- Neuroimmune Mechanisms Underlying Post-acute Sequelae of SARS-CoV-2 (PASC) Pain, Predictions from a Ligand-Receptor Interactome.Current rheumatology reports · 2023Review
- Small Extracellular Vesicles From Spared Nerve Injury Model and Sham Control Mice Differentially Regulate Gene Expression in Primary Microglia.The journal of pain · 2023Article
- Sex-dependent differences in the genomic profile of lingual sensory neurons in naïve and tongue-tumor bearing mice.Scientific reports · 2023Article
- Role of Microglia in Neuropathic Pain.Cureus · 2023Review
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Microarray expression profiles reveal substantial changes in gene expression in the ipsilateral dorsal horn of the spinal cord in response to three peripheral nerve injury models of neuropathic pain. However, only 54 of the 612 regulated genes are commonly expressed across all the neuropathic pain models. Many of the commonly regulated transcripts are immune related and include the complement components C1q, C3, and C4, which we find are expressed only by microglia. C1q and C4 are, moreover, the most strongly regulated of all 612 regulated genes. In addition, we find that the terminal complement component C5 and the C5a receptor (C5aR) are upregulated in spinal microglia after peripheral nerve injury. Mice null for C5 had reduced neuropathic pain sensitivity, excluding C3a as a pain effector. C6-deficient rats, which cannot form the membrane attack complex, have a normal neuropathic pain phenotype. However, C5a applied intrathecally produces a dose-dependent, slow-onset cold pain in naive animals. Furthermore, a C5aR peptide antagonist reduces cold allodynia in neuropathic pain models. We conclude that induction of the complement cascade in spinal cord microglia after peripheral nerve injury contributes to neuropathic pain through the release and action of the C5a anaphylatoxin peptide.
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Registered trials
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.