ArticleMediators of inflammation2013
Chronic pain treatment: the influence of tricyclic antidepressants on serotonin release and uptake in mast cells.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Morphometry of Mast Cells in the Tongue Tissues of the White Rats under Stress Conditions.Bulletin of experimental biology and medicine · 2026Article
- The Anti-Inflammatory Potential of Tricyclic Antidepressants (TCAs): A Novel Therapeutic Approach to Atherosclerosis Pathophysiology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Use of Zebrafish as a Non-traditional Model Organism in Translational Pain Research: The Knowns and the Unknowns.Current neuropharmacology · 2022Article
- Involvement of Mast Cells in the Pathophysiology of Pain.Frontiers in cellular neuroscience · 2021Article
- Neuroendocrine factors: The missing link in non‑melanoma skin cancer (Review).Oncology reports · 2017Review
- TRPA1 polymorphisms in chronic and complete spinal cord injury patients with neuropathic pain: a pilot study.Spinal cord series and cases · 2017Article
- Stress-induced mast cell activation in glabrous and hairy skin.Mediators of inflammation · 2014Article
- Effects of acupuncture knife on inflammatory factors and pain in third lumbar vertebrae transverse process syndrome model rats.Evidence-based complementary and alternative medicine : eCAM · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of serotonin (5-HT) in chronic pain mechanisms is established. 5-HT inhibits central painful stimuli, but recent data suggests that 5-HT could also enhance pain stimulus from the periphery, where mast cells play an important role. We aimed in our study to clarify the influence of selected tricyclic antidepressants (TCAs) on mast cell function: secretion, uptake, and reuptake of 5-HT, that could interfere with 5-HT levels and in this way contribute to the generation of pain. As an experimental model, we used isolated rat peritoneal mast cells and incubated them with selected TCAs (clomipramine, amitriptyline, doxepin, and imipramine) under different experimental conditions. 5-HT release, uptake, and reuptake were determined spectrofluorometrically. We showed that TCAs were able to inhibit 5-HT secretion from mast cells, as well as uptake of exogenous 5-HT and reuptake of secreted 5-HT back into mast cells. The effects of TCAs were concentration dependent; higher concentrations of TCAs inhibited the secretion of 5-HT induced by compound 48/80, whereas lower concentrations of TCAs inhibited 5-HT uptake. The most effective TCA was halogenated clomipramine. As TCAs are well introduced in chronic pain treatment, the insight into mechanisms of action is important for an understanding of their effect in various pain conditions.
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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.