ArticlePharmaceuticals (Basel, Switzerland)2022
Investigation of the Mechanisms of Tramadol-Induced Seizures in Overdose in the Rat.
Article in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Sex-specific pharmacovigilance signals and time-to-onset patterns of drug-related myoclonus and epileptic seizures: a real-world pharmacovigilance analysis.Frontiers in pharmacology · 2026Article
- Clinical Profile and Drugs of Abuse Identified among People who Use Drugs Admitted to a Tertiary Hospital in the Philippines using a Validated LC-QTOF/MS Method.Acta medica Philippina · 2025Article
- Recent Advances in Conductive Polymers-Based Electrochemical Sensors for Biomedical and Environmental Applications.Polymers · 2024Review
- An Update on Psychoactive Substances: Pharmacology and Toxicology Issues.Pharmaceuticals (Basel, Switzerland) · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tramadol overdose is frequently associated with the onset of seizures, usually considered as serotonin syndrome manifestations. Recently, the serotoninergic mechanism of tramadol-attributed seizures has been questioned. This study’s aim was to identify the mechanisms involved in tramadol-induced seizures in overdose in rats. The investigations included (1) the effects of specific pretreatments on tramadol-induced seizure onset and brain monoamine concentrations, (2) the interaction between tramadol and γ-aminobutyric acid (GABA)A receptors in vivo in the brain using positron emission tomography (PET) imaging and 11C-flumazenil. Diazepam abolished tramadol-induced seizures, in contrast to naloxone, cyproheptadine and fexofenadine pretreatments. Despite seizure abolishment, diazepam significantly enhanced tramadol-induced increase in the brain serotonin (p < 0.01), histamine (p < 0.01), dopamine (p < 0.05) and norepinephrine (p < 0.05). No displacement of 11C-flumazenil brain kinetics was observed following tramadol administration in contrast to diazepam, suggesting that the observed interaction was not related to a competitive mechanism between tramadol and flumazenil at the benzodiazepine-binding site. Our findings do not support the involvement of serotoninergic, histaminergic, dopaminergic, norepinephrine or opioidergic pathways in tramadol-induced seizures in overdose, but they strongly suggest a tramadol-induced allosteric change of the benzodiazepine-binding site of GABAA receptors. Management of tramadol-poisoned patients should take into account that tramadol-induced seizures are mainly related to a GABAergic pathway.
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