ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Expression of central glucocorticoid receptors after peripheral nerve injury contributes to neuropathic pain behaviors in rats.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 118 citations in OpenAlex.
- The effect of preoperative dexamethasone on pain 1 year after lumbar disc surgery: a follow-up study.BMC anesthesiology · 2016Trial
- Glucocorticoid receptor dynamics and neuroinflammation in chronic restraint stress-induced mechanical allodynia in female rats.The journal of pain · 2025Article
- The effects of lowering barometric pressure on pain behavior and the stress hormone in mice with neuropathic pain.PloS one · 2025Article
- Glucocorticoid signaling mediates stress-induced migraine-like behaviors in a preclinical mouse model.Cephalalgia : an international journal of headache · 2024Article
- The Underlying Mechanisms of Sleep Deprivation Exacerbating Neuropathic Pain.Nature and science of sleep · 2023Review
- Glucocorticoid Receptor/HCN4 Channels Interaction in Spinal Dorsal Horn Participates in the Regulation of Neuropathic Pain after Peripheral Nerve Injury in Rats.Bulletin of experimental biology and medicine · 2022Article
- Exploring the Therapeutic Potential of Targeting Purinergic and Orexinergic Receptors in Alcoholic Neuropathy.Neurotoxicity research · 2022Review
- Effect of m-Trifluoromethyl-diphenyl diselenide on the Pain-Depression Dyad Induced by Reserpine: Insights on Oxidative Stress, Apoptotic, and Glucocorticoid Receptor Modulation.Molecular neurobiology · 2021Article
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- Does epigenetic 'memory' of early-life stress predispose to chronic pain in later life? A potential role for the stress regulatorPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Hypothalamic-pituitary-adrenal axis function in traumatic spinal cord injury-related neuropathic pain: a case-control study.Journal of endocrinological investigation · 2019Article
- Corticosterone Upregulates Gene and Protein Expression of Catecholamine Markers in Organotypic Brainstem Cultures.International journal of molecular sciences · 2019Article
- Analgesic effects of ASP3662, a novel 11β-hydroxysteroid dehydrogenase 1 inhibitor, in rat models of neuropathic and dysfunctional pain.British journal of pharmacology · 2018Article
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- Neuropathic pain drives anxiety behavior in mice, results consistent with anxiety levels in diabetic neuropathy patients.Pain reports · 2018Article
- Maternal separation stress leads to resilience against neuropathic pain in adulthood.Neurobiology of stress · 2018Article
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- Glucocorticoid-Potentiated Spinal Microglia Activation Contributes to Preoperative Anxiety-Induced Postoperative Hyperalgesia.Molecular neurobiology · 2017Article
- Stress-Induced Chronic Visceral Pain of Gastrointestinal Origin.Frontiers in systems neuroscience · 2017Review
5 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Peripheral glucocorticoid receptors (GRs) play a significant role in the anti-inflammatory effects of glucocorticoids; however, the role of central GRs in nociceptive behaviors after peripheral nerve injury (neuropathic pain behaviors) remains unknown. Here we show that the development of neuropathic pain behaviors (thermal hyperalgesia and mechanical allodynia) induced by chronic constriction nerve injury (CCI) in rats was attenuated by either the GR antagonist RU38486 (4 = 2 > 1 = 0.5 microg) or a GR antisense oligonucleotide administered intrathecally twice daily for postoperative days 1-6. The development of thermal hyperalgesia and mechanical allodynia after CCI also was prevented in adrenalectomized rats, whereas the GR agonist dexamethasone (100 microg/kg) given subcutaneously twice daily for postoperative day 1-6 restored CCI-induced neuropathic pain behaviors in the adrenalectomized rats. Mechanistically, CCI induced a time-dependent and region-specific expression of neuronal GRs primarily within the spinal cord dorsal horn ipsilateral to nerve injury, which showed a time course parallel to that of the development of neuropathic pain behaviors. Moreover, the expression of neuronal GR after CCI was mediated in part through an elevated spinal level of interleukin-6 (IL-6) and protein kinase Cgamma (PKCgamma), because intrathecal treatment with an IL-6 antiserum, a PKC inhibitor (cheryrithrine), or PKCgamma knock-out substantially reduced the expression of neuronal GRs as well as neuropathic pain behaviors after CCI. These findings indicate a central role of neuronal GRs in the mechanisms of neuropathic pain behaviors in rats and suggest a potential role for GR antagonists in clinical management of neuropathic pain.
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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.