ArticleEuropean journal of pharmacology2010
Sustained morphine treatment augments prostaglandin E2-evoked calcitonin gene-related peptide release from primary sensory neurons in a PKA-dependent manner.
Article in European journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Neuroinflammatory crosstalk in migraine: consolidated activity of rizatriptan and meloxicam in suppressing CGRP-induced nociception and COX-mediated inflammation.Inflammopharmacology · 2025Review
- Tissue Regeneration: The Dark Side of Opioids.International journal of molecular sciences · 2021Review
- Thiazolidine Derivatives Attenuate Carrageenan-Induced Inflammatory Pain in Mice.Drug design, development and therapy · 2021Article
- TRPV1 Channel Activated by the PGE2/EP4 Pathway Mediates Spinal Hypersensitivity in a Mouse Model of Vertebral Endplate Degeneration.Oxidative medicine and cellular longevity · 2021Article
- Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion.Frontiers in neuroscience · 2021Article
- Molecular mechanisms underlying the actions of arachidonic acid-derived prostaglandins on peripheral nociception.Journal of neuroinflammation · 2020Review
- The need for new acutely acting antimigraine drugs: moving safely outside acute medication overuse.The journal of headache and pain · 2019Review
- The Benzimidazole Derivatives, B1 (Frontiers in neuroscience · 2019Article
- Delta Opioid Receptor Expression and Function in Primary Afferent Somatosensory Neurons.Handbook of experimental pharmacology · 2018Review
- Repeated morphine treatment-mediated hyperalgesia, allodynia and spinal glial activation are blocked by co-administration of a selective cannabinoid receptor type-2 agonist.Journal of neuroimmunology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tissue damage leads to pain sensitization due to peripheral and central release of excitatory mediators such as prostaglandin E₂ (PGE₂). PGE₂ sensitizes spinal pain neurotransmitter such as calcitonin gene-related peptide (CGRP) release via activation of cyclic AMP (cAMP)/protein kinase A (PKA)-dependent signaling mechanisms. Our previous data demonstrate that sustained morphine pretreatment sensitizes adenylyl cyclase(s) (AC) toward the direct stimulator, forskolin, in cultured primary sensory neurons (AC superactivation). In the present work we investigated the hypothesis that morphine pretreatment also sensitizes ACs toward Gs-protein-coupled excitatory modulators (such as PGE₂), leading to augmented PKA-dependent CGRP release from PGE₂-stimulated primary sensory dorsal root ganglion (DRG) neurons. Our results show that sustained morphine treatment potentiated PGE₂-mediated cAMP formation and augmented PGE₂-evoked CGRP release from cultured primary sensory neurons in a PKA-dependent manner. Our data suggest that attenuation of AC superactivation in primary sensory neurons may prevent the development of opioid-induced 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.