ArticleEpilepsia2025
kcnb1 loss of function in zebrafish causes neurodevelopmental and epileptic disorders associated with γ-aminobutyric acid dysregulation.
Article in Epilepsia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- kcnb1 loss of function in zebrafish causes neurodevelopmental and epileptic disorders associated with γ-aminobutyric acid dysregulation.Epilepsia · 2025Article
- Seizure-like behavior and hyperactivity in napb knockout zebrafish as a model for autism and epilepsy.Scientific reports · 2025Article
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8 authors.
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Abstract
objectiveKCNB1 encodes an α-subunit of the delayed-rectifier voltage-dependent potassium channel K
methodsThis study presents the phenotypic analysis of a kcnb1 knockout zebrafish model, obtained by CRISPR/Cas9 (Clustered Regularly Interspaced Short Palindromic Repeats) mutagenesis. Through a combination of immunohistochemistry, behavioral assays, electrophysiological recordings, and neurotransmitter quantifications, we have characterized the expression, function, and impact of this kcnb1 LOF model at early stages of development.
resultsIn wild-type (WT) larval zebrafish, kcnb1 was found in various regions of the central nervous system and in diverse cell subtypes including neurons, oligodendrocytes, and microglial cells. Both kcnb1 SIGNIFICANCE: We conclude that kcnb1 knockout in zebrafish leads to early onset phenotypic features reminiscent of DEEs, affecting neuronal functions and primarily inhibitory pathways in developing embryonic and larval brains. This study highlights the relevance of this model for investigating developmental neuronal signaling pathways in KCNB1-related DEEs.
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