ArticleMolecular neurobiology2014
Activation of extracellular signal-regulated kinase1/2 in the medial prefrontal cortex contributes to stress-induced hyperalgesia.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Repetitive Transcranial Magnetic Stimulation of the mPFC Ameliorates Stress-Induced Hyperalgesia by Alleviating Microglia Activation in Rats.Brain and behavior · 2026Article
- 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
- Activation of Calcium/Calmodulin-Dependent Kinase II in the Medial Prefrontal Cortex Mediates Spinal Cord Injury-Related Cognitive and Affective Changes.Brain and behavior · 2025Article
- Early-life exposure to selective serotonin reuptake inhibitors: Long-term effects on pain and affective comorbidities.The European journal of neuroscience · 2022Review
- TNF-Alpha as an Initiator of Allodynia and Anxiety-Like Behaviors in a Preclinical Model of PTSD and Comorbid Pain.Frontiers in psychiatry · 2021Article
- Role of the Prefrontal Cortex in Pain Processing.Molecular neurobiology · 2019Review
- Anxiety-induced hyperalgesia in female rats is mediated by cholecystokinin 2 receptor in rostral ventromedial medulla and spinal 5-hydroxytryptamine 2B receptor.Journal of pain research · 2019Article
- Effects of Post-Weaning Chronic Stress on Nociception, Spinal Cord μ-Opioid, and α2-Adrenergic Receptors Expression in Rats and Their Offspring.Journal of molecular neuroscience : MN · 2018Article
- Sex Differences in Nociceptin/Orphanin FQ Peptide Receptor-Mediated Pain and Anxiety Symptoms in a Preclinical Model of Post-traumatic Stress Disorder.Frontiers in psychiatry · 2018Article
- Single-Prolonged Stress: A Review of Two Decades of Progress in a Rodent Model of Post-traumatic Stress Disorder.Frontiers in psychiatry · 2018Review
- Glucocorticoid-Potentiated Spinal Microglia Activation Contributes to Preoperative Anxiety-Induced Postoperative Hyperalgesia.Molecular neurobiology · 2017Article
- Crosstalk between Activated Microglia and Neurons in the Spinal Dorsal Horn Contributes to Stress-induced Hyperalgesia.Scientific reports · 2016Article
- Corticotrigeminal Projections from the Insular Cortex to the Trigeminal Caudal Subnucleus Regulate Orofacial Pain after Nerve Injury via Extracellular Signal-Regulated Kinase Activation in Insular Cortex Neurons.Frontiers in cellular neuroscience · 2015Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stressful stimuli can exacerbate persistent pain disorder. However, the underlying mechanism is still unknown. Here, to reveal the underlying mechanism for stressful stimuli-induced hyperalgesia in chronic pain, we investigated the effect of extracellular signal-regulated kinase1/2 (ERK1/2) activation on pain hypersensitivity using single-prolonged stress (SPS) model, complete Freund's adjuvant (CFA) model and SPS + CFA model. The experimental results revealed significantly reduced paw withdrawal threshold in the SPS, CFA, and SPS + CFA group compared with the control group. However, the increased phosphorylation of ERK1/2 in the medial prefrontal cortex (mPFC) was observed in the SPS- or SPS + CFA-exposed group but not the CFA group compared with control group. There was also a significant increase in mPFC ERK1/2 phosphorylation and mechanical allodynia after SPS + CFA treatment compared to SPS or CFA treatment alone. Furthermore, inhibiting ERK1/2 phosphorylation by microinjection of U0126, a MAPK kinase (MEK) inhibitor, into the mPFC attenuated SPS + CFA- and SPS- but not CFA-induced mechanical allodynia, anxiety-like behavior, and cognitive impairments. These results suggest that the activation of ERK1/2 in the mPFC may contribute to the process of stress-induced cognitive and emotional disorders, leading to an increase in pain sensitivity.
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