ArticleScientific reports2016
Interferon alpha inhibits spinal cord synaptic and nociceptive transmission via neuronal-glial interactions.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The trial behind it
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Who cites it
41 citing papers in PubMed, 80 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Molecular mechanisms and therapeutic perspectives in vulvodynia: From current evidence to future investigations.Cell reports. Medicine · 2026Review
- Type I IFNs enhance human dorsal root ganglion nociceptor excitability and induce TRPV1 sensitization.JCI insight · 2025Article
- Astrocytic P2X7 receptor in retrosplenial cortex drives electroacupuncture analgesia.Purinergic signalling · 2025Article
- Neurotransmitter and metabolic effects of interferon-alpha in association with decreased striatal dopamine in a non-human primate model of cytokine-Induced depression.Brain, behavior, and immunity · 2025Article
- Article
- Eukaryotic initiation factors: central factor associating mRNA translational plasticity during neuropathic pain progression.Frontiers in neurology · 2025Review
- Innate immune pathway activated mesenchymal stromal cells improve function and histologic outcomes in a rodent osteoarthritis model.Frontiers in bioengineering and biotechnology · 2025Article
- Innate immune pathway activation to modulate mesenchymal stromal cell (MSC) interactions with synovium and cartilage.Frontiers in bioengineering and biotechnology · 2025Article
- Decoding Fibromyalgia: Genetic Insights into Gut and Immune System Interactions.Journal of pain research · 2025Article
- A microglia-containing cerebral organoid model to study early life immune challenges.Brain, behavior, and immunity · 2025Article
- Oleic acid released by sensory neurons inhibits TRPV1-mediated thermal hypersensitivity via GPR40.iScience · 2024Article
- STINGing away the pain: the role of interferon-stimulated genes.The Journal of clinical investigation · 2024Article
- Induction of antiviral interferon-stimulated genes by neuronal STING promotes the resolution of pain in mice.The Journal of clinical investigation · 2024Article
- Microglial STING activation alleviates nerve injury-induced neuropathic pain in male but not female mice.Brain, behavior, and immunity · 2024Article
- Vinorelbine causes a neuropathic pain-like state in mice via STING and MNK1 signaling associated with type I interferon induction.iScience · 2024Article
- Emerging Roles of Type-I Interferons in Neuroinflammation, Neurological Diseases, and Long-Haul COVID.International journal of molecular sciences · 2022Review
- Activation of GPR183 by 7The Journal of pharmacology and experimental therapeutics · 2022Article
- STING-ing Pain: How Can Pro-inflammatory Signaling Attenuate Pain?Neuroscience bulletin · 2021Article
- Single-cell RNA-seq analysis reveals compartment-specific heterogeneity and plasticity of microglia.iScience · 2021Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
It is well known that interferons (IFNs), such as type-I IFN (IFN-α) and type-II IFN (IFN-γ) are produced by immune cells to elicit antiviral effects. IFNs are also produced by glial cells in the CNS to regulate brain functions. As a proinflammatory cytokine, IFN-γ drives neuropathic pain by inducing microglial activation in the spinal cord. However, little is known about the role of IFN-α in regulating pain sensitivity and synaptic transmission. Strikingly, we found that IFN-α/β receptor (type-I IFN receptor) was expressed by primary afferent terminals in the superficial dorsal horn that co-expressed the neuropeptide CGRP. In the spinal cord IFN-α was primarily expressed by astrocytes. Perfusion of spinal cord slices with IFN-α suppressed excitatory synaptic transmission by reducing the frequency of spontaneous excitatory postsynaptic current (sEPSCs). IFN-α also inhibited nociceptive transmission by reducing capsaicin-induced internalization of NK-1 and phosphorylation of extracellular signal-regulated kinase (ERK) in superficial dorsal horn neurons. Finally, spinal (intrathecal) administration of IFN-α reduced inflammatory pain and increased pain threshold in naïve rats, whereas removal of endogenous IFN-α by a neutralizing antibody induced hyperalgesia. Our findings suggest a new form of neuronal-glial interaction by which IFN-α, produced by astrocytes, inhibits nociceptive transmission in the spinal cord.
Identifiers
What OpenQuestion holds
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.