ArticleFrontiers in pharmacology2017
Nicotine Elicits Convulsive Seizures by Activating Amygdalar Neurons.
Article in Frontiers in pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.
- Maternal smoking during pregnancy and childhood seizure: a systematic review and meta-analysis.BMC pregnancy and childbirth · 2026Pooled it
- A Systematic Literature Review of E-Cigarette-Related Illness and Injury: Not Just for the Respirologist.International journal of environmental research and public health · 2020Pooled it
- Toxicological and pharmacodynamic evaluation of Nixodine-S [(S)-6-Methylnicotine] relative to (S)-nicotine.Toxicology reports · 2026Article
- Anticonvulsant Potential of 1-Aryl-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinolines: Insights from Strychnine and Nicotine Models in In Vivo and In Silico Studies.Pharmaceuticals (Basel, Switzerland) · 2025Article
- The effect of acetylcholinesterase inhibitor rivastigmine in pentylenetetrazole-induced kindling model of epilepsy in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Chemoarchitectural signatures of subcortical shape alterations in generalized epilepsy.Communications biology · 2024Article
- Nicotine modifies cocaine responding in a concurrent self-administration model.Drug and alcohol dependence · 2023Article
- Review
- Altered neuronal activity in the ventromedial prefrontal cortex drives nicotine intake escalation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Article
- The role of heat-not-burn, snus and other nicotine-containing products as interventions for epileptic patients who take phenytoin and smoke cigarettes.Toxicology reports · 2022Article
- Molecular Recognition of Nerve Agents and Their Organophosphorus Surrogates: Toward Supramolecular Scavengers and Catalysts.Chemistry (Weinheim an der Bergstrasse, Germany) · 2021Review
- Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord.International journal of molecular sciences · 2021Article
- Cholinergic Signaling, Neural Excitability, and Epilepsy.Molecules (Basel, Switzerland) · 2021Review
- Chinese Herbal Medicine for Treating Epilepsy.Frontiers in neuroscience · 2021Review
- The role of nicotinic acetylcholine receptors in alcohol-related behaviors.Brain research bulletin · 2020Review
- Mechanism Underlying Organophosphate Paraoxon-Induced Kinetic Tremor.Neurotoxicity research · 2019Article
- Seizure Susceptibility in E-cigarette Users: Navigating the Clinical Management and Public Health Considerations.Substance use : research and treatmentReview
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 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nicotinic acetylcholine (nACh) receptors are implicated in the pathogenesis of epileptic disorders; however, the mechanisms of nACh receptors in seizure generation remain unknown. Here, we performed behavioral and immunohistochemical studies in mice and rats to clarify the mechanisms underlying nicotine-induced seizures. Treatment of animals with nicotine (1-4 mg/kg, i.p.) produced motor excitement in a dose-dependent manner and elicited convulsive seizures at 3 and 4 mg/kg. The nicotine-induced seizures were abolished by a subtype non-selective nACh antagonist, mecamylamine (MEC). An α7 nACh antagonist, methyllycaconitine, also significantly inhibited nicotine-induced seizures whereas an α4β2 nACh antagonist, dihydro-β-erythroidine, affected only weakly. Topographical analysis of Fos protein expression, a biological marker of neural excitation, revealed that a convulsive dose (4 mg/kg) of nicotine region-specifically activated neurons in the piriform cortex, amygdala, medial habenula, paratenial thalamus, anterior hypothalamus and solitary nucleus among 48 brain regions examined, and this was also suppressed by MEC. In addition, electric lesioning of the amygdala, but not the piriform cortex, medial habenula and thalamus, specifically inhibited nicotine-induced seizures. Furthermore, microinjection of nicotine (100 and 300 μg/side) into the amygdala elicited convulsive seizures in a dose-related manner. The present results suggest that nicotine elicits convulsive seizures by activating amygdalar neurons mainly via α7 nACh receptors.
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.