ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Phosphatidylinositol 3-kinase is a key mediator of central sensitization in painful inflammatory conditions.
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 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.
- Bone metastasis and pain research through the dual lens of bibliometrics and bioinformatics: knowledge structure, frontiers, and core pathway analysis (2015-2024).Frontiers in medicine · 2025Pooled it
- Extracellular Vesicles in Migraine: Biomarkers and Therapeutics.Molecular neurobiology · 2026Review
- Spinal TREM2/PI3K/Akt signal axis elicits microglial activation and aggravates bone cancer pain.Journal of anesthesia and translational medicine · 2025Article
- The Proteomic Analysis of Chronic Migraine Exosomes Reveals Disease Patterns and Potential Biomarkers.Molecular neurobiology · 2025Article
- Electroacupuncture Reduced Fibromyalgia-Pain-like Behavior through Inactivating Transient Receptor Potential V1 and Interleukin-17 in Intermittent Cold Stress Mice Model.Brain sciences · 2024Article
- Involvement of HDAC2-mediated kcnq2/kcnq3 genes transcription repression activated by EREG/EGFR-ERK-Runx1 signaling in bone cancer pain.Cell communication and signaling : CCS · 2024Article
- Advances in Neuropathic Pain Research: Selected Intracellular Factors as Potential Targets for Multidirectional Analgesics.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Dopamine receptor D2 regulates GLUA1-containing AMPA receptor trafficking and central sensitization through the PI3K signaling pathway in a male rat model of chronic migraine.The journal of headache and pain · 2022Article
- Dual PI3Kδ/γ Inhibitor Duvelisib Prevents Development of Neuropathic Pain in Model of Paclitaxel-Induced Peripheral Neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Spinal AMPA receptors: Amenable players in central sensitization for chronic pain therapy?Channels (Austin, Tex.) · 2021Review
- PI3Kγ/AKT Signaling in High Molecular Weight Hyaluronan (HMWH)-Induced Anti-Hyperalgesia and Reversal of Nociceptor Sensitization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Manual Acupuncture at ST37 Modulates TRPV1 in Rats with Acute Visceral Hyperalgesia via Phosphatidylinositol 3-Kinase/Akt Pathway.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Modulation of Pathological Pain by Epidermal Growth Factor Receptor.Frontiers in pharmacology · 2021Review
- Impact of Hepatoma-Derived Growth Factor Blockade on Resiniferatoxin-Induced Neuropathy.Neural plasticity · 2021Article
- Systems and Circuits Linking Chronic Pain and Circadian Rhythms.Frontiers in neuroscience · 2021Review
- Calcium Permeable-AMPA Receptors and Excitotoxicity in Neurological Disorders.Frontiers in neural circuits · 2021Review
- Pellino1 regulates neuropathic pain as well as microglial activation through the regulation of MAPK/NF-κB signaling in the spinal cord.Journal of neuroinflammation · 2020Article
- An Investigation of the Molecular Mechanisms Underlying the Analgesic Effect of Jakyak-Gamcho Decoction: A Network Pharmacology Study.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Sonic Hedgehog Signaling Contributes to Chronic Post-Thoracotomy Pain via Activating BDNF/TrkB Pathway in Rats.Journal of pain research · 2020Article
- Post-surgical inhibition of phosphatidylinositol 3-kinase attenuates the plantar incision-induced postoperative pain behavior via spinal Akt activation in male mice.BMC neuroscience · 2019Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Here, we show that phosphatidylinositol 3-kinase (PI3K) is a key player in the establishment of central sensitization, the spinal cord phenomenon associated with persistent afferent inputs and contributing to chronic pain states. We demonstrated electrophysiologically that PI3K is required for the full expression of spinal neuronal wind-up. In an inflammatory pain model, intrathecal administration of LY294002 [2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one], a potent PI3K inhibitor, dose-dependently inhibited pain-related behavior. This effect was correlated with a reduction of the phosphorylation of ERK (extracellular signal-regulated kinase) and CaMKII (calcium/calmodulin-dependent protein kinase II). In addition, we observed a significant decrease in the phosphorylation of the NMDA receptor subunit NR2B, decreased translocation to the plasma membrane of the GluR1 (glutamate receptor 1) AMPA receptor subunit in the spinal cord, and a reduction of evoked neuronal activity as measured using c-Fos immunohistochemistry. Our study suggests that PI3K is a major factor in the expression of central sensitization after noxious inflammatory stimuli.
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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.