ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Interferon-gamma is a critical modulator of CB(2) cannabinoid receptor signaling during neuropathic pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Cannabinoid Receptors: An Update on Cell Signaling, Pathophysiological Roles and Therapeutic Opportunities in Neurological, Cardiovascular, and Inflammatory Diseases.International journal of molecular sciences · 2020Pooled it
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Interferon-γ Mitigates Oxaliplatin-Induced Neurotoxicity: Analogies With Connexin 43.CNS neuroscience & therapeutics · 2026Article
- Endocannabinoid Modulation in Headache: Mechanisms, Models, and Translational Therapies.Cells · 2026Review
- Dual Role of the Spinal Endocannabinoid System in Response to Noxious Stimuli: Antinociceptive Pathways and Neuropathic Pain Mechanisms.International journal of molecular sciences · 2025Review
- Cannabinoid Receptor 2 (CB2) in Macrophages: A Promising Clinical Target for Immune Disorders.International journal of molecular sciences · 2025Review
- The Hunt for the Putative Epoxyeicosatrienoic Acid Receptor.ACS chemical biology · 2025Review
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- Mirror-Image Pain Update: Complex Interactions Between Central and Peripheral Mechanisms.Molecular neurobiology · 2024Review
- Cannabinoids for Acute Pain Management: Approaches and Rationale.Current pain and headache reports · 2024Review
- Review
- Melatonin Induces Analgesic Effects through MTResearch (Washington, D.C.) · 2024Article
- Hydrogen Sulfide Interacting with Cannabinoid 2 Receptors during Sciatic Nerve Injury-Induced Neuropathic Pain.Antioxidants (Basel, Switzerland) · 2023Article
- Beneficial Effects and Potential Mechanisms of Tai Chi on Lower Limb Osteoarthritis: A Biopsychosocial Perspective.Chinese journal of integrative medicine · 2023Review
- Microglial Cannabinoid CBInternational journal of molecular sciences · 2023Review
- Interferon-gamma and neuropathy: balance between pain and neuroprotection.Neural regeneration research · 2022Article
- Inflammation and Nitro-oxidative Stress as Drivers of Endocannabinoid System Aberrations in Mood Disorders and Schizophrenia.Molecular neurobiology · 2022Review
- Article
- "The Two Sides of the Same Coin"-Medical Cannabis, Cannabinoids and Immunity: Pros and Cons Explained.Pharmaceutics · 2022Review
- Effect of traditional Chinese manual therapy on alleviating pain and dysfunction of lumbar disc herniation: a randomized controlled pilot study.American journal of translational research · 2022Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Nerve injuries often lead to neuropathic pain syndrome. The mechanisms contributing to this syndrome involve local inflammatory responses, activation of glia cells, and changes in the plasticity of neuronal nociceptive pathways. Cannabinoid CB(2) receptors contribute to the local containment of neuropathic pain by modulating glial activation in response to nerve injury. Thus, neuropathic pain spreads in mice lacking CB(2) receptors beyond the site of nerve injury. To further investigate the mechanisms leading to the enhanced manifestation of neuropathic pain, we have established expression profiles of spinal cord tissues from wild-type and CB(2)-deficient mice after nerve injury. An enhanced interferon-gamma (IFN-gamma) response was revealed in the absence of CB(2) signaling. Immunofluorescence stainings demonstrated an IFN-gamma production by astrocytes and neurons ispilateral to the nerve injury in wild-type animals. In contrast, CB(2)-deficient mice showed neuronal and astrocytic IFN-gamma immunoreactivity also in the contralateral region, thus matching the pattern of nociceptive hypersensitivity in these animals. Experiments in BV-2 microglia cells revealed that transcriptional changes induced by IFN-gamma in two key elements for neuropathic pain development, iNOS (inducible nitric oxide synthase) and CCR2, are modulated by CB(2) receptor signaling. The most direct support for a functional involvement of IFN-gamma as a mediator of CB(2) signaling was obtained with a double knock-out mouse strain deficient in CB(2) receptors and IFN-gamma. These animals no longer show the enhanced manifestations of neuropathic pain observed in CB(2) knock-outs. These data clearly demonstrate that the CB(2) receptor-mediated control of neuropathic pain is IFN-gamma dependent.
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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.