ReviewFrontiers in physiology2015
The role of nicotinic acetylcholine receptors in autosomal dominant nocturnal frontal lobe epilepsy.
Review in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 97 citations in OpenAlex.
- Juvenile myoclonic epilepsy heterogeneity uncovered: Z-mapped imaging endophenotypes of cortical and subcortical structures and their clinical, cognitive and psychiatric features.Brain communications · 2026Article
- Emerging Role of Tripartite Synaptic Transmission in the Pathomechanism of Autosomal-Dominant Sleep-Related Hypermotor Epilepsy.International journal of molecular sciences · 2025Review
- Juvenile Myoclonic Epilepsy Imaging Endophenotypes and Relationship With Cognition and Resting-State EEG.Human brain mapping · 2025Article
- α4β2The Journal of physiology · 2025Article
- Tonic-clonic seizures induce hypersomnia and suppress rapid eye movement sleep in mouse models of epilepsy.Sleep advances : a journal of the Sleep Research Society · 2025Article
- Smoking and epilepsy in national health interview survey: a cross-sectional study.Frontiers in human neuroscience · 2025Article
- Pearls & Oy-sters: Exquisite Response of Sleep-Related Hypermotor Epilepsy to a Nicotine Patch.Neurology · 2024Article
- Characterization of 13 Novel Genetic Variants in Genes Associated with Epilepsy: Implications for Targeted Therapeutic Strategies.Molecular diagnosis & therapy · 2024Article
- Novel interplay between agonist and calcium binding sites modulates drug potentiation of α7 acetylcholine receptor.Cellular and molecular life sciences : CMLS · 2024Article
- Structural bases for stoichiometry-selective calcium potentiation of a neuronal nicotinic receptor.British journal of pharmacology · 2024Article
- Pathogenic genes implicated in sleep-related hypermotor epilepsy: a research progress update.Frontiers in neurology · 2024Review
- Vitamin BNature cell biology · 2024Article
- Review
- Case report: A young man with non-rapid eye movement parasomnias in aFrontiers in neurology · 2023Article
- How do smoking, vaping, and nicotine affect people with epilepsy and seizures? A scoping review protocol.PloS one · 2023Article
- Genetic Variant in Nicotinic Receptor α4-Subunit Causes Sleep-Related Hyperkinetic Epilepsy via Increased Channel Opening.International journal of molecular sciences · 2022Article
- Anti-Ovarian Cancer Conotoxins Identified fromMolecules (Basel, Switzerland) · 2022Article
- Rare variants in GABRG2 associated with sleep-related hypermotor epilepsy.Journal of neurology · 2022Article
- Can rodent models elucidate the pathomechanisms of genetic epilepsy?British journal of pharmacology · 2022Review
- A novel missense creatine mutant ofTranslational pediatrics · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is a focal epilepsy with attacks typically arising in the frontal lobe during non-rapid eye movement (NREM) sleep. It is characterized by clusters of complex and stereotyped hypermotor seizures, frequently accompanied by sudden arousals. Cognitive and psychiatric symptoms may be also observed. Approximately 12% of the ADNFLE families carry mutations on genes coding for subunits of the heteromeric neuronal nicotinic receptors (nAChRs). This is consistent with the widespread expression of these receptors, particularly the α4β2(*) subtype, in the neocortex and thalamus. However, understanding how mutant nAChRs lead to partial frontal epilepsy is far from being straightforward because of the complexity of the cholinergic regulation in both developing and mature brains. The relation with the sleep-waking cycle must be also explained. We discuss some possible pathogenetic mechanisms in the light of recent advances about the nAChR role in prefrontal regions as well as the studies carried out in murine models of ADNFLE. Functional evidence points to alterations in prefrontal GABA release, and the synaptic unbalance probably arises during the cortical circuit maturation. Although most of the available functional evidence concerns mutations on nAChR subunit genes, other genes have been recently implicated in the disease, such as KCNT1 (coding for a Na(+)-dependent K(+) channel), DEPD5 (Disheveled, Egl-10 and Pleckstrin Domain-containing protein 5), and CRH (Corticotropin-Releasing Hormone). Overall, the uncertainties about both the etiology and the pathogenesis of ADNFLE point to the current gaps in our knowledge the regulation of neuronal networks in the cerebral cortex.
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