ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Epilepsy-Associated KCNQ2 Channels Regulate Multiple Intrinsic Properties of Layer 2/3 Pyramidal Neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Kcnq2 R213 knock-in mice reveal variant- and region-specific mechanisms underlying self-limited familial neonatal-infantile epilepsy and early infantile developmental and epileptic encephalopathy.Acta neuropathologica communications · 2026Article
- Mislocalization of KCNQ2 Channels as a Pathogenic Mechanism in KCNQ2 Developmental and Epileptic Encephalopathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Human iPSC-derived glutamatergic neurons with pathogenic KCNQ2 variants display hyperactive bursting phenotypes.Neurobiology of disease · 2025Article
- Glial KCNQ KNeuron · 2024Article
- Rare genetic brain disorders with overlapping neurological and psychiatric phenotypes.Nature reviews. Neurology · 2024Review
- Neuromodulator regulation and emotions: insights from the crosstalk of cell signaling.Frontiers in molecular neuroscience · 2024Review
- Voltage-gated potassium channels and genetic epilepsy.Frontiers in neurology · 2024Review
- Phox2b-expressing neurons contribute to breathing problems in Kcnq2 loss- and gain-of-function encephalopathy models.Nature communications · 2023Article
- The PFC-LH-VTA pathway contributes to social deficits in IRSp53-mutant mice.Molecular psychiatry · 2023Article
- KCNQ2/3 Gain-of-Function Variants and Cell Excitability: Differential Effects in CA1 versus L2/3 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Kv7/KCNQ potassium channels in cortical hyperexcitability and juvenile seizure-related death in Ank2-mutant mice.Nature communications · 2023Article
- Biocytin-Labeling in Whole-Cell Recording: Electrophysiological and Morphological Properties of Pyramidal Neurons in CYLD-Deficient Mice.Molecules (Basel, Switzerland) · 2023Article
- Degeneracy in epilepsy: multiple routes to hyperexcitable brain circuits and their repair.Communications biology · 2023Review
- Gene mutations in comorbidity of epilepsy and arrhythmia.Journal of neurology · 2023Review
- A pilot investigation of differential hydroxymethylation levels in patient-derived neural stem cells implicates altered cortical development in bipolar disorder.Frontiers in psychiatry · 2023Article
- KCNQ2 channels regulate the population activity of neonatal GABAergic neuronsFrontiers in neurology · 2023Article
- Mouse models of Kcnq2 dysfunction.Epilepsia · 2022Review
- Article
- Transcriptional Activation, Deactivation and Rebound Patterns in Cortex, Hippocampus and Amygdala in Response to Ketamine Infusion in Rats.Frontiers in molecular neuroscience · 2022Article
- Clinical Study of 30 NovelFrontiers in molecular neuroscience · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
KCNQ2 potassium channels are critical for normal brain function, as both loss-of-function and gain-of-function KCNQ2 variants can lead to various forms of neonatal epilepsy. Despite recent progress, the full spectrum of consequences as a result of KCNQ2 dysfunction in neocortical pyramidal neurons is still unknown. Here, we report that conditional ablation of Kcnq2 from mouse neocortex leads to hyperexcitability of layer 2/3 (L2/3) pyramidal neurons, exhibiting an increased input resistance and action potential frequency, as well as a reduced medium afterhyperpolarization (mAHP), a conductance partly mediated by KCNQ2 channels. Importantly, we show that introducing the KCNQ2 loss-of-function variant KCNQ2 SIGNIFICANCE STATEMENT: KCNQ2 channels are critical for the development of normal brain function, as KCNQ2 variants could lead to epileptic encephalopathy. However, the role of KCNQ2 channels in regulating the properties of neocortical neurons is largely unexplored. Here, we find that Kcnq2 ablation or loss-of-function at subthreshold membrane potentials leads to increased neuronal excitability of neocortical layer 2/3 (L2/3) pyramidal neurons. We also demonstrate that Kcnq2 ablation unexpectedly leads to a larger action potential amplitude. Importantly, we propose the Na
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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.