ArticleCells2019
Defective Excitatory/Inhibitory Synaptic Balance and Increased Neuron Apoptosis in a Zebrafish Model of Dravet Syndrome.
Article in Cells, 2019. 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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Who cites it
25 citing papers in PubMed.
- Critical neuronal avalanches arise from excitation-inhibition balanced spontaneous activity.iScience · 2026Article
- Whole-brain cellular-resolution functional network properties of seizure susceptibility.bioRxiv : the preprint server for biology · 2026Article
- MMP-2/9 inhibition modulates sharp wave abundance, inhibitory proteoglycan sulfation, and fear memory in juvenile zebrafish: relevance to affective disorders.Molecular psychiatry · 2025Article
- Modulation of NMDA receptor signaling and zinc chelation prevent seizure-like events in a zebrafish model of SLC13A5 epilepsy.PLoS biology · 2025Article
- Enhanced proconvulsant sensitivity, not spontaneous rapid swimming activity, is a robust correlate ofbioRxiv : the preprint server for biology · 2025Article
- Socially induced plasticity of the posterior tuberculum and motor behavior in zebrafish (Danio rerio).The Journal of experimental biology · 2024Article
- Zebrafish models of human-duplicatedbioRxiv : the preprint server for biology · 2024Article
- Decreased GABA levels during development result in increased connectivity in the larval zebrafish tectum.bioRxiv : the preprint server for biology · 2024Article
- Coupling of Sharp Wave Events between Zebrafish Hippocampal and Amygdala Homologs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Article
- Fenfluramine increases survival and reduces markers of neurodegeneration in a mouse model of Dravet syndrome.Epilepsia open · 2024Article
- Epilepsy insights revealed by intravital functional optical imaging.Frontiers in neurology · 2024Review
- Testing of putative antiseizure medications in a preclinical Dravet syndrome zebrafish model.Brain communications · 2024Article
- Testing of putative antiseizure drugs in a preclinical Dravet syndrome zebrafish model.bioRxiv : the preprint server for biology · 2023Article
- Imaging Approaches to Investigate Pathophysiological Mechanisms of Brain Disease in Zebrafish.International journal of molecular sciences · 2023Review
- Volumetric light sheet imaging with adaptive optics correction.Biomedical optics express · 2023Article
- Multimodal Characterization of Seizures in Zebrafish Larvae.Biomedicines · 2022Article
- Synaptic dysfunction connects autism spectrum disorder and sleep disturbances: A perspective from studies in model organisms.Sleep medicine reviews · 2022Review
- Use of Zebrafish Models to Boost Research in Rare Genetic Diseases.International journal of molecular sciences · 2021Review
- Inhibitory synaptic transmission is impaired at higher extracellular CaScientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dravet syndrome is a type of severe childhood epilepsy that responds poorly to current anti-epileptic drugs. In recent years, zebrafish disease models with Scn1Lab sodium channel deficiency have been generated to seek novel anti-epileptic drug candidates, some of which are currently undergoing clinical trials. However, the spectrum of neuronal deficits observed following Scn1Lab depletion in zebrafish larvae has not yet been fully explored. To fill this gap and gain a better understanding of the mechanisms underlying neuron hyperexcitation in Scn1Lab-depleted larvae, we analyzed neuron activity in vivo using combined local field potential recording and transient calcium uptake imaging, studied the distribution of excitatory and inhibitory synapses and neurons as well as investigated neuron apoptosis. We found that Scn1Lab-depleted larvae displayed recurrent epileptiform seizure events, associating massive synchronous calcium uptakes and ictal-like local field potential bursts. Scn1Lab-depletion also caused a dramatic shift in the neuronal and synaptic balance toward excitation and increased neuronal death. Our results thus provide in vivo evidence suggesting that Scn1Lab loss of function causes neuron hyperexcitation as the result of disturbed synaptic balance and increased neuronal apoptosis.
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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.