ArticleNeuropharmacology2014
Neuropathic plasticity in the opioid and non-opioid actions of dynorphin A fragments and their interactions with bradykinin B2 receptors on neuronal activity in the rat spinal cord.
Article in Neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- Understanding of Spinal Wide Dynamic Range Neurons and Their Modulation on Pathological Pain.Journal of pain research · 2024Review
- Spinal orexin A attenuates opioid-induced mechanical hypersensitivity in the rat.The Korean journal of pain · 2022Article
- Endogenous Opioid Dynorphin Is a Potential Link between Traumatic Brain Injury, Chronic Pain, and Substance Use Disorder.Journal of neurotrauma · 2022Review
- Multifunctional Opioid-Derived Hybrids in Neuropathic Pain: Preclinical Evidence, Ideas and Challenges.Molecules (Basel, Switzerland) · 2020Review
- Cortical Regulation of Nociception of the Trigeminal Nucleus Caudalis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Neuronal-Glial Interactions Maintain Chronic Neuropathic Pain after Spinal Cord Injury.Neural plasticity · 2017Review
- Cyclic non-opioid dynorphin A analogues for the bradykinin receptors.Bioorganic & medicinal chemistry letters · 2016Article
- Various modifications of the amphipathic dynorphin A pharmacophore for rat brain bradykinin receptors.Chemical biology & drug design · 2016Article
- Epigenetic regulation of spinal cord gene expression contributes to enhanced postoperative pain and analgesic tolerance subsequent to continuous opioid exposure.Molecular pain · 2016Article
- Modification of amphipathic non-opioid dynorphin A analogues for rat brain bradykinin receptors.Bioorganic & medicinal chemistry letters · 2015Article
- Opioid-induced hyperalgesia in chronic pain patients and the mitigating effects of gabapentin.Frontiers in pharmacology · 2015Review
- Structure-activity relationships of non-opioid [des-Arg(7)]-dynorphin A analogues for bradykinin receptors.Bioorganic & medicinal chemistry letters · 2014Article
- Effect of adenoviral delivery of prodynorphin gene on experimental inflammatory pain induced by formalin in rats.International journal of clinical and experimental medicine · 2014Article
- Blockade of non-opioid excitatory effects of spinal dynorphin A at bradykinin receptors.Receptors & clinical investigationArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Dynorphin A is an endogenous opioid peptide derived from the precursor prodynorphin. The proteolytic fragment dynorphin A (1-17) exhibits inhibitory effects via opioid receptors. Paradoxically, the activity of the dynorphin system increases with chronic pain and neuropathy is associated with the up-regulation of dynorphin biosynthesis. Dynorphin A (1-17) is cleaved in vivo to produce a non-opioid fragment, dynorphin A (2-17). Previously, a mechanism by which the non-opioid fragment promotes pain through agonist action at bradykinin receptors was revealed. Bradykinin receptor expression is up-regulated after nerve injury and both a truncated version of non-opioid fragment dynorphin A (2-17), referred to as 'Ligand 10', and novel bradykinin receptor antagonist 'Ligand 14', are known to bind to the bradykinin receptor. Here we show that Ligand 10 facilitates the response of wide dynamic range (WDR) neurons to innocuous and noxious mechanical stimuli in neuropathic, but not naïve, animals, while Ligand 14 exhibits inhibitory effects in neuropathic animals only. Furthermore, we reveal an inhibitory effect of Ligand 14 in naïve animals by pre-dosing with either Ligand 10 or a 5-HT3 receptor agonist to reflect activation of descending excitatory drives. Thus remarkably, by mimicking pro-excitatory pharmacological changes that occur after nerve injury in a naïve animal, we induce a state whereby the inhibitory actions of Ligand 14 are now effective. Ultimately our data support an increasing number of studies that suggest that blocking spinal bradykinin receptors may have a therapeutic potential in chronic pain states, here, in particular, in 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.