ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Stress induces a switch of intracellular signaling in sensory neurons in a model of generalized 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 92 papers, 1 of them a synthesis that pooled it.
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Who cites it
92 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- 2015 AAHA/AAFP pain management guidelines for dogs and cats.Journal of feline medicine and surgery · 2015Guideline
- Trial
- Article
- Glucocorticoid receptor dynamics and neuroinflammation in chronic restraint stress-induced mechanical allodynia in female rats.The journal of pain · 2025Article
- Hyperalgesic Priming in the Transition From Acute to Chronic Pain: Focus on Different Models and the Molecular Mechanisms Involved.Journal of pain research · 2025Review
- The Effects of Acute Stress on Evoked-cortical Connectivity through Wide-field Optical Mapping of Neural and Hemodynamic Signals.Experimental neurobiology · 2024Article
- Exploring the link between pediatric headaches and environmental noise exposure.BMC pediatrics · 2024Review
- Effect of curcumin on formalin-induced muscle pain in male rats: role of local cyclooxygenase system.Veterinary research forum : an international quarterly journal · 2024Article
- 2023 AAFP/IAAHPC feline hospice and palliative care guidelines.Journal of feline medicine and surgery · 2023Review
- The Biology of Stress Intolerance in Patients with Chronic Pain-State of the Art and Future Directions.Journal of clinical medicine · 2023Review
- AAV-glycine receptor α3 alleviates CFA-induced inflammatory pain by downregulating ERK phosphorylation and proinflammatory cytokine expression in SD rats.Molecular medicine (Cambridge, Mass.) · 2023Article
- High-fat diet causes mechanical allodynia in the absence of injury or diabetic pathology.Scientific reports · 2022Article
- Duration of Reduction in Enduring Stress-Induced Hyperalgesia Via FKBP51 Inhibition Depends on Timing of Administration Relative to Traumatic Stress Exposure.The journal of pain · 2022Article
- Neuroendocrine Stress Axis-Dependence of Duloxetine Analgesia (Anti-Hyperalgesia) in Chemotherapy-Induced Peripheral Neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Unpredictable Sound Stress Model Causes Migraine-Like Behaviors in Mice With Sexual Dimorphism.Frontiers in pharmacology · 2022Article
- Inhibitory effects of biofeedback electrostimulation therapy on pain and cortisol levels in chronic neuropathic pain: A randomized-controlled trial.Turkish journal of physical medicine and rehabilitation · 2021Article
- Opioid-Induced Hyperalgesic Priming in Single Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Excitation-Inhibition Imbalance Leads to Alteration of Neuronal Coherence and Neurovascular Coupling under Acute Stress.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Article
- Neurovascular Coupling under Chronic Stress Is Modified by Altered GABAergic Interneuron Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Stress dramatically exacerbates pain in diseases such as fibromyalgia and rheumatoid arthritis, but the underlying mechanisms are unknown. We tested the hypothesis that stress causes generalized hyperalgesia by enhancing pronociceptive effects of immune mediators. Rats exposed to nonhabituating sound stress exhibited no change in mechanical nociceptive threshold, but showed a marked increase in hyperalgesia evoked by local injections of prostaglandin E(2) or epinephrine. This enhancement, which developed more than a week after exposure to stress, required concerted action of glucocorticoids and catecholamines at receptors located in the periphery on sensory afferents. The altered response to pronociceptive mediators involved a switch in coupling of their receptors from predominantly stimulatory to inhibitory G-proteins (G(s) to G(i)), and for prostaglandin E(2), emergence of novel dependence on protein kinase C epsilon. Thus, an important mechanism in generalized pain syndromes may be stress-induced coactivation of the hypothalamo-pituitary-adrenal and sympathoadrenal axes, causing a long-lasting alteration in intracellular signaling pathways, enabling normally innocuous levels of immune mediators to produce chronic hyperalgesia.
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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.