ArticleNeural plasticity2026
A JNK-Regulated and IL-1β-Dependent Astrocyte-Neuron Signaling Pathway in the Spinal Dorsal Horn is Essential for Stress-Induced Hyperalgesia.
Article in Neural plasticity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Repetitive Transcranial Magnetic Stimulation of the mPFC Ameliorates Stress-Induced Hyperalgesia by Alleviating Microglia Activation in Rats.Brain and behavior · 2026Article
- Neuroimmune regulation of post-traumatic bone regeneration: focus on inflammatory switching and functional recovery.Frontiers in immunology · 2026Review
- A JNK-Regulated and IL-1β-Dependent Astrocyte-Neuron Signaling Pathway in the Spinal Dorsal Horn is Essential for Stress-Induced Hyperalgesia.Neural plasticity · 2026Article
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3 authors.
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Abstract
Various forms of mild stress may exacerbate pain in patients with chronic pain disorders, though the underlying mechanism remains unclear. Astrocyte activation in the spinal dorsal horn plays a predominant role in stress and pain. The present study investigated the neuron-astrocyte interactions in the spinal dorsal horn in post-traumatic stress disorder (PTSD)-induced hyperalgesia using a single-prolonged stress (SPS) model, a Complete Freund's Adjuvant (CFA) model and an SPS + CFA model. Animals were tested for mechanical withdrawal threshold (MWT) of the paw after SPS, CFA and SPS + CFA. SPS + CFA group induced significantly increased mechanical allodynia compared with the SPS or CFA group. We tested the hypothesis that IL-1β contributes to signaling between astrocytes and neurons in stress-induced hyperalgesia (SIH). Immunohistochemical data showed that there was an upregulation of glial fibrillary acidic proteins (GFAPs, a marker of astrocyte) and Fos (a marker of neuron) in SIH. Immunohistochemical data showed specific localization of IL-1β to astrocyte, but not to microglia and neurons and a neuronal localization of the IL-1β receptor (IL-1RI) with NMDAR2B (NR2B). Enzyme immunoassay analysis showed that IL-1β release was dependent on c-Jun N-terminal kinase (JNK) activation in astrocyte. The JNK inhibitor SP600125 suppressed IL-1β release. SP600125 and IL-1RI blockade with IL-1ra resulted in a restoration of behavioral nociceptive thresholds. Our results showed that the IL-1β-dependent, JNK-regulated astrocyte-neuron signaling pathway mediated the astroglia component of pain maintenance in SIH.
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