ArticlePain2012
Calcium/calmodulin dependent kinase II contributes to persistent central neuropathic pain following spinal cord injury.
Article in Pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 64 citations in OpenAlex.
- Calcium/calmodulin-dependent protein kinase II inhibition using tatCN19o ameliorates spinal cord ischemia associated with aortic surgery.The Journal of thoracic and cardiovascular surgery · 2026Article
- Single-cell transcriptomics reveals probiotic reversal of neonatal morphine-induced gene disruptions underlying adolescent pain hypersensitivity.Communications biology · 2025Article
- Cytokines reprogram airway sensory neurons in asthma.bioRxiv : the preprint server for biology · 2024Article
- Chemogenetic Attenuation of Acute Nociceptive Signaling Enhances Functional Outcomes Following Spinal Cord Injury.Journal of neurotrauma · 2024Article
- The role and mechanism of esketamine in preventing and treating remifentanil-induced hyperalgesia based on the NMDA receptor-CaMKII pathway.Open life sciences · 2024Article
- Diabetes-Induced Amplification of Nociceptive DRG Neuron Output by Upregulation of Somatic T-Type CaBiomolecules · 2023Article
- Excitatory and inhibitory neuronal signaling in inflammatory and diabetic neuropathic pain.Molecular medicine (Cambridge, Mass.) · 2023Review
- Spinal Cord Injury Provoked Neuropathic Pain and Spasticity, and Their GABAergic Connection.Neurospine · 2022Article
- The Roles of Superoxide on At-Level Spinal Cord Injury Pain in Rats.International journal of molecular sciences · 2021Article
- Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.Cellular and molecular neurobiology · 2020Review
- Increased calcium-mediated cerebral processes after peripheral injury: possible role of the brain in complex regional pain syndrome.The Korean journal of pain · 2020Article
- Galanin Receptor 2 Is Involved in Galanin-Induced Analgesic Effect by Activating PKC and CaMKII in the Nucleus Accumbens of Inflammatory Pain Rats.Frontiers in neuroscience · 2020Article
- Long Noncoding RNA H19 Induces Neuropathic Pain by Upregulating Cyclin-Dependent Kinase 5-Mediated Phosphorylation of cAMP Response Element Binding Protein.Journal of pain research · 2020Article
- Article
- TRPV1 channel contributes to remifentanil-induced postoperative hyperalgesia via regulation of NMDA receptor trafficking in dorsal root ganglion.Journal of pain research · 2019Article
- Effects of intrathecal bupivacaine on the NR2B/CaMKIIα/CREB signaling pathway in the rat lumbar spinal cord.Molecular medicine reports · 2018Article
- Chemokine receptor CXCR4 regulates CaMKII/CREB pathway in spinal neurons that underlies cancer-induced bone pain.Scientific reports · 2017Article
- Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury.Neural plasticity · 2017Review
- Blocking mammalian target of rapamycin (mTOR) improves neuropathic pain evoked by spinal cord injury.Translational neuroscience · 2016Article
- A store-operated calcium channel inhibitor attenuates collagen-induced arthritis.British journal of pharmacology · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Chronic central neuropathic pain after central nervous system injuries remains refractory to therapeutic interventions. A novel approach would be to target key intracellular signaling proteins that are known to contribute to continued activation by phosphorylation of kinases, transcription factors, and/or receptors that contribute to changes in membrane excitability. We demonstrate that one signaling kinase, calcium/calmodulin-dependent kinase II (CaMKII), is critical in maintaining aberrant dorsal horn neuron hyperexcitability in the neuropathic pain condition after spinal cord injury (SCI). After contusion SCI at spinal level T10, activated CaMKII (phosphorylated, pCaMKII) expression is significantly upregulated in the T7/8 spinal dorsal horn in neurons, but not glial cells, and in oligodendrocytes in the dorsal column in the same rats that displayed at-level mechanical allodynia. Furthermore, identified spinothalamic neurons demonstrated significant increases of pCaMKII after SCI compared to sham-treated control animals. However, neither astrocytes nor microglia showed pCaMKII expression in either sham-treated or SCI rats. To demonstrate causality, treatment of SCI rats with KN-93, which prevents CaMKII activation, significantly attenuated at-level mechanical allodynia and aberrant wide dynamic range neuronal activity evoked by brush, pressure, and pinch stimuli and a graded series of von Frey stimuli, respectively. Persistent CaMKII activation contributes to chronic central neuropathic pain by mechanisms that involve maintained hyperexcitability of wide dynamic range dorsal horn neurons. Furthermore, targeting key signaling proteins is a novel, useful therapeutic strategy for treating chronic central 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.