ReviewThe Journal of physiology2013
Ion channels in genetic and acquired forms of epilepsy.
Review in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
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.
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
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 161 citations in OpenAlex.
- Genetic determinants of common epilepsies: a meta-analysis of genome-wide association studies.The Lancet. Neurology · 2014Pooled it
- Altered oligodendroglial cell development and increased myelination in SCN2A gain-of-function-linked epilepsy.Acta neuropathologica communications · 2026Article
- Rethinking cortical hypertrophy in temporal lobe epilepsy.Brain : a journal of neurology · 2026Review
- From metabolic intermediary to neurotransmitter: purinergic signaling in neurophysiology and vulnerability of brain circuits.Bioscience reports · 2026Review
- Bacterial Communication: The Possible Role of Quorum Sensing, Quantum Mechanics, and Quantum Tunneling.Metabolites · 2026Review
- Review
- Novel 3-Methoxypropanamide Derivatives as Potential Antiseizure and Antinociceptive Agents: Experimental Evidence from In Vitro and In Vivo Studies.Journal of medicinal chemistry · 2026Article
- Neurologist's Black Swan: Molecular Basis of Prenatal Seizures.International journal of molecular sciences · 2025Review
- Diverse species of animal models in epilepsy research: Progress and perspectives.Zoological research · 2025Review
- A primary mechanism for efficacy of the ketogenic diet may be energy repletion at the tripartite synapse.Journal of neural engineering · 2025Article
- Developmental mechanisms underlying pediatric epilepsy.Frontiers in neurology · 2025Review
- Review
- Metabolic aspects of genetic ion channel epilepsies.Journal of neurochemistry · 2024Review
- Indian Hedgehog (IHh) Protein and COX-2 as Biomarkers to Define the Mechanism of Epilepsy and Gastrointestinal Problems as Comorbid Medical Illnesses in Autism Spectrum Disorder: Combining ROC Curves to Improve Diagnostic Values.Journal of clinical medicine · 2024Article
- Alterations in DNA 5-hydroxymethylation patterns in the hippocampus of an experimental model of chronic epilepsy.Neurobiology of disease · 2024Article
- Novel Alaninamide Derivatives with Drug-like Potential for Development as Antiseizure and Antinociceptive Therapies─In Vitro and In Vivo Characterization.ACS chemical neuroscience · 2024Article
- Analysis of the action mechanisms and targets of herbal anticonvulsants highlights opportunities for therapeutic engagement with refractory epilepsy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Single shot detection of alterations across multiple ionic currents from assimilation of cell membrane dynamics.Scientific reports · 2024Article
- Functional Analysis of NMDAR Subunit Components in Postsynaptic Currents of Identified Cells and Synapses in Brain Slices.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Schiff Bases: A Captivating Scaffold with Potential Anticonvulsant Activity.Mini reviews in medicinal chemistry · 2024Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 6 institutions in 3 countries.
Funding
Abstract
Genetic mutations causing dysfunction of both voltage- and ligand-gated ion channels make a major contribution to the cause of many different types of familial epilepsy. Key mechanisms comprise defective Na(+) channels of inhibitory neurons, or GABA(A) receptors affecting pre- or postsynaptic GABAergic inhibition, or a dysfunction of different types of channels at axon initial segments. Many of these ion channel mutations have been modelled in mice, which has largely contributed to the understanding of where and how the ion channel defects lead to neuronal hyperexcitability. Animal models of febrile seizures or mesial temporal epilepsy have shown that dendritic K(+) channels, hyperpolarization-activated cation channels and T-type Ca(2+) channels play important roles in the generation of seizures. For the latter, it has been shown that suppression of their function by pharmacological mechanisms or in knock-out mice can antagonize epileptogenesis. Defects of ion channel function are also associated with forms of acquired epilepsy. Autoantibodies directed against ion channels or associated proteins, such as K(+) channels, LGI1 or NMDA receptors, have been identified in epileptic disorders that can largely be included under the term limbic encephalitis which includes limbic seizures, status epilepticus and psychiatric symptoms. We conclude that ion channels and associated proteins are important players in different types of genetic and acquired epilepsies. Nevertheless, the molecular bases for most common forms of epilepsy are not yet clear, and evidence to be discussed indicates just how much more we need to understand about the complex mechanisms that underlie epileptogenesis.
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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.