ArticleMolecular pain2012
Serotonin-induced hypersensitivity via inhibition of catechol O-methyltransferase activity.
Article in Molecular pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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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.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Involvement of Intestinal Enteroendocrine Cells in Neurological and Psychiatric Disorders.Biomedicines · 2022Review
- Analytical methodologies for sensing catechol-Journal of pharmaceutical analysis · 2021Review
- Probiotics Affect One-Carbon Metabolites and Catecholamines in a Genetic Rat Model of Depression.Molecular nutrition & food research · 2018Article
- S-Adenosyl Methionine and Transmethylation Pathways in Neuropsychiatric Diseases Throughout Life.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Catechol-O-methyltransferase activity in erythrocytes from patients with eating disorders.Eating and weight disorders : EWD · 2016Article
- Article
- Generation and characterization of humanized mice carrying COMT158 Met/Val alleles.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Epistasis and complex neuropsychiatric phenotypes.Psychiatry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The subcutaneous and systemic injection of serotonin reduces cutaneous and visceral pain thresholds and increases responses to noxious stimuli. Different subtypes of 5-hydroxytryptamine (5-HT) receptors are suggested to be associated with different types of pain responses. Here we show that serotonin also inhibits catechol O-methyltransferase (COMT), an enzyme that contributes to modultion the perception of pain, via non-competitive binding to the site bound by catechol substrates with a binding affinity comparable to the binding affinity of catechol itself (K(i) = 44 μM). Using computational modeling, biochemical tests and cellular assays we show that serotonin actively competes with the methyl donor S-adenosyl-L-methionine (SAM) within the catalytic site. Binding of serotonin to the catalytic site inhibits the access of SAM, thus preventing methylation of COMT substrates. The results of in vivo animal studies show that serotonin-induced pain hypersensitivity in mice is reduced by either SAM pretreatment or by the combined administration of selective antagonists for β(2)- and β(3)-adrenergic receptors, which have been previously shown to mediate COMT-dependent pain signaling. Our results suggest that inhibition of COMT via serotonin binding contributes to pain hypersensitivity, providing additional strategies for the treatment of clinical pain conditions.
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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.