ReviewMolecular neurobiology2015
Regulation of membrane excitability: a convergence on voltage-gated sodium conductance.
Review in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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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.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Potential Effect of Belladonna in the Management of Convulsions in Zebrafish (Annals of neurosciences · 2026Article
- Identification of CNTN2 as a genetic modifier of PIGA-CDG in a family with incomplete penetrance and in Drosophila.American journal of human genetics · 2025Article
- The Anticancer Journey of Liquiritin: Insights into Its Mechanisms and Therapeutic Prospects.Current medicinal chemistry · 2025Review
- Voltage Gated Ion Channels and Sleep.The Journal of membrane biology · 2024Review
- Disuse-Induced Muscle Fatigue: Facts and Assumptions.International journal of molecular sciences · 2024Review
- Lidocaine Inhibits Rat Prostate Cancer Cell Invasiveness and Voltage-Gated Sodium Channel Expression in Plasma Membrane.The Journal of membrane biology · 2024Article
- Characterization of NaLife science alliance · 2024Article
- Thermal acclimation and habitat-dependent differences in temperature robustness of a crustacean motor circuit.Frontiers in cellular neuroscience · 2023Article
- Article
- High-Frequency Neuronal Bursting is Essential for Circadian and Sleep Behaviors inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Transcriptome Analysis Reveals Higher Levels of Mobile Element-Associated Abnormal Gene Transcripts in Temporal Lobe Epilepsy Patients.Frontiers in genetics · 2021Article
- Article
- Alternative Splicing by NOVA Factors: From Gene Expression to Cell Physiology and Pathology.International journal of molecular sciences · 2020Review
- Pumilio Regulates Sleep Homeostasis in Response to Chronic Sleep Deprivation inFrontiers in neuroscience · 2020Article
- Exciting Complexity: The Role of Motor Circuit Elements in ALS Pathophysiology.Frontiers in neuroscience · 2020Review
- Article
- Propofol inhibits the voltage-gated sodium channel NaChBac at multiple sites.The Journal of general physiology · 2018Article
- The NaFrontiers in pharmacology · 2018Review
- Reciprocal voltage sensor-to-pore coupling leads to potassium channel C-type inactivation.Scientific reports · 2016Article
- Impaired Axonal Na(+) Current by Hindlimb Unloading: Implication for Disuse Neuromuscular Atrophy.Frontiers in physiology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The voltage-gated sodium channel (Nav) plays a key role in regulation of neuronal excitability. Aberrant regulation of Nav expression and/or function can result in an imbalance in neuronal activity which can progress to epilepsy. Regulation of Nav activity is achieved by coordination of a multitude of mechanisms including RNA alternative splicing and translational repression. Understanding of these regulatory mechanisms is complicated by extensive genetic redundancy: the mammalian genome encodes ten Navs. By contrast, the genome of the fruitfly, Drosophila melanogaster, contains just one Nav homologue, encoded by paralytic (DmNa v ). Analysis of splicing in DmNa v shows variants exhibit distinct gating properties including varying magnitudes of persistent sodium current (INaP). Splicing by Pasilla, an identified RNA splicing factor, alters INaP magnitude as part of an activity-dependent mechanism. Enhanced INaP promotes membrane hyperexcitability that is associated with seizure-like behaviour in Drosophila. Nova-2, a mammalian Pasilla homologue, has also been linked to splicing of Navs and, moreover, mouse gene knockouts display seizure-like behaviour.Expression level of Navs is also regulated through a mechanism of translational repression in both flies and mammals. The translational repressor Pumilio (Pum) can bind to Na v transcripts and repress the normal process of translation, thus regulating sodium current (INa) density in neurons. Pum2-deficient mice exhibit spontaneous EEG abnormalities. Taken together, aberrant regulation of Nav function and/or expression is often epileptogenic. As such, a better understanding of regulation of membrane excitability through RNA alternative splicing and translational repression of Navs should provide new leads to treat epilepsy.
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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.