ArticleThe European journal of neuroscience2008
Neurotoxic catecholamine metabolite in nociceptors contributes to painful peripheral neuropathy.
Article in The European journal of neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- The differences in the anatomy of the thoracolumbar and sacral autonomic outflow are quantitative.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2024Review
- The Catecholaldehyde Hypothesis for the Pathogenesis of Catecholaminergic Neurodegeneration: What We Know and What We Do Not Know.International journal of molecular sciences · 2021Review
- Biological Evaluation ofACS omega · 2021Article
- CAR-T Cell Therapy: Mechanism, Management, and Mitigation of Inflammatory Toxicities.Frontiers in immunology · 2021Review
- Potential Patient-Reported Toxicities With Disulfiram Treatment in Late Disseminated Lyme Disease.Frontiers in medicine · 2020Article
- The antinociceptive effects of ferulic acid on neuropathic pain: involvement of descending monoaminergic system and opioid receptors.Oncotarget · 2016Article
- Review
- Modulation of imidazoline I2 binding sites by CR4056 relieves postoperative hyperalgesia in male and female rats.British journal of pharmacology · 2014Article
- Diabetes-causing gene, kruppel-like factor 11, modulates the antinociceptive response of chronic ethanol intake.Alcoholism, clinical and experimental research · 2014Article
- Independent contributions of alcohol and stress axis hormones to painful peripheral neuropathy.Neuroscience · 2013Article
- Dorsal root ganglion neurons innervating pelvic organs in the mouse express tyrosine hydroxylase.Neuroscience · 2012Article
- CR4056, a new analgesic I2 ligand, is highly effective against bortezomib-induced painful neuropathy in rats.Journal of pain research · 2012Article
- Analgesic efficacy of CR4056, a novel imidazoline-2 receptor ligand, in rat models of inflammatory and neuropathic pain.Journal of pain research · 2011Article
- Inhibitors of catechol-O-methyltransferase sensitize mice to pain.British journal of pharmacology · 2010Article
- Alcohol consumption enhances antiretroviral painful peripheral neuropathy by mitochondrial mechanisms.The European journal of neuroscience · 2010Article
- Lidocaine 5% patch for localized neuropathic pain: progress for the patient, a new approach for the physician.Clinical pharmacology : advances and applications · 2010Article
- Neurotoxic catecholamine metabolite in nociceptors contributes to painful peripheral neuropathy.The European journal of neuroscience · 2009Article
- Probiotics attenuate alcohol-induced muscle mechanical hyperalgesia: Preliminary observations.Molecular painArticle
Corrections and comments
- Correction · 2009-11-25Error in Data · Error in Results and/or Conclusions ·
- Erratum issued
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The neurotoxic effects of catecholamine metabolites have been implicated in neurodegenerative diseases. As some sensory neurons express tyrosine hydroxylase and monoamine oxidase (MAO), we investigated the potential contribution of catecholamine metabolites to neuropathic pain in a model of alcoholic neuropathy. The presence of catecholamines in sensory neurons is supported by capsaicin-stimulated epinephrine release, an effect enhanced in ethanol-fed rats. mRNA for enzymes in dorsal root ganglia involved in catecholamine uptake and metabolism, dopamine beta-hydroxylase and MAO-A, were decreased by neonatal administration of capsaicin. Ethanol-induced hyperalgesia was attenuated by systemic and local peripheral administration of inhibitors of MAO-A, reduction of norepinephrine transporter (NET) in sensory neurons and a NET inhibitor. Finally, intradermal injection of 3,4-dihydroxyphenylglycolaldehyde (DOPEGAL), a neurotoxic MAO-A catecholamine metabolite, produced robust mechanical hyperalgesia. These observations suggest that catecholamines in nociceptors are metabolized to neurotoxic products by MAO-A, which can cause neuronal dysfunction underlying neuropathic pain.
Indexed as
Identifiers
What OpenQuestion holds
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.