ArticleGenes, brain, and behavior2014
Deletion of the Kv2.1 delayed rectifier potassium channel leads to neuronal and behavioral hyperexcitability.
Article in Genes, brain, and behavior, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Intellectual Disability and Potassium Channelopathies: A Systematic Review.Frontiers in genetics · 2020Pooled it
- Disease spectrum of nonconvulsive status epilepticus in children: A study based on clinical subtype characteristics and prognostic stratification.Epileptic disorders : international epilepsy journal with videotape · 2026Article
- Unveiling sleep disturbances in KCNB1-related disorders: Insights from a cohort of 78 individuals.Epilepsia open · 2026Article
- A silent Kv channel subunit shapes PV neuron action potential waveform and short-term synaptic plasticity during high-frequency firing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A silent Kv channel subunit shapes PV neuron action potential waveform and short-term synaptic plasticity during high-frequency firing.bioRxiv : the preprint server for biology · 2025Article
- Transgenic mouse models of sodium and potassium channelopathies in epilepsy: insights into disease mechanisms and therapeutics.Bioscience reports · 2025Review
- Kv2/Kv6.4 Heteromeric Potassium Channels Are Expressed in Spinal Motoneurons and Localized at C-Bouton Synapses.The European journal of neuroscience · 2025Article
- Distinct Electrophysiological Signatures Define Neuronal Subtypes in the Fasciola Cinereum.bioRxiv : the preprint server for biology · 2025Article
- Common Genomic and Proteomic Alterations Related to Disturbed Neural Oscillatory Activity in Schizophrenia.International journal of molecular sciences · 2025Review
- kcnb1 loss of function in zebrafish causes neurodevelopmental and epileptic disorders associated with γ-aminobutyric acid dysregulation.Epilepsia · 2025Article
- A forward genetic screen identifies potassium channel essentiality in SHH medulloblastoma maintenance.Developmental cell · 2025Article
- The Electrically Silent Kv5.1 Subunit Forms Heteromeric Kv2 Channels in Cortical Neurons and Confers Distinct Functional Properties.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Kv2.1 negatively regulates Reissner fiber development.Frontiers in cell and developmental biology · 2025Article
- Abnormal cytoskeletal remodeling but normal neuronal excitability in a mouse model of the recurrent developmental and epileptic encephalopathy-susceptibility KCNB1-p.R312H variant.Communications biology · 2024Article
- The involvement of KTranslational psychiatry · 2024Review
- Article
- Innovative drug discovery strategies in epilepsy: integrating next-generation syndrome-specific mouse models to address pharmacoresistance and epileptogenesis.Expert opinion on drug discovery · 2024Review
- Article
- Altered neurological and neurobehavioral phenotypes in a mouse model of the recurrent KCNB1-p.R306C voltage-sensor variant.Neurobiology of disease · 2024Article
- Mono-allelic KCNB2 variants lead to a neurodevelopmental syndrome caused by altered channel inactivation.American journal of human genetics · 2024Article
29 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
The Kv2.1 delayed rectifier potassium channel exhibits high-level expression in both principal and inhibitory neurons throughout the central nervous system, including prominent expression in hippocampal neurons. Studies of in vitro preparations suggest that Kv2.1 is a key yet conditional regulator of intrinsic neuronal excitability, mediated by changes in Kv2.1 expression, localization and function via activity-dependent regulation of Kv2.1 phosphorylation. Here we identify neurological and behavioral deficits in mutant (Kv2.1(-/-) ) mice lacking this channel. Kv2.1(-/-) mice have grossly normal characteristics. No impairment in vision or motor coordination was apparent, although Kv2.1(-/-) mice exhibit reduced body weight. The anatomic structure and expression of related Kv channels in the brains of Kv2.1(-/-) mice appear unchanged. Delayed rectifier potassium current is diminished in hippocampal neurons cultured from Kv2.1(-/-) animals. Field recordings from hippocampal slices of Kv2.1(-/-) mice reveal hyperexcitability in response to the convulsant bicuculline, and epileptiform activity in response to stimulation. In Kv2.1(-/-) mice, long-term potentiation at the Schaffer collateral - CA1 synapse is decreased. Kv2.1(-/-) mice are strikingly hyperactive, and exhibit defects in spatial learning, failing to improve performance in a Morris Water Maze task. Kv2.1(-/-) mice are hypersensitive to the effects of the convulsants flurothyl and pilocarpine, consistent with a role for Kv2.1 as a conditional suppressor of neuronal activity. Although not prone to spontaneous seizures, Kv2.1(-/-) mice exhibit accelerated seizure progression. Together, these findings suggest homeostatic suppression of elevated neuronal activity by Kv2.1 plays a central role in regulating neuronal network function.
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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.