ArticleProceedings of the National Academy of Sciences of the United States of America2008
Contribution of KCNQ2 and KCNQ3 to the medium and slow afterhyperpolarization currents.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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86 citing papers in PubMed, 141 citations in OpenAlex.
- TDP-43-dependent mis-splicing of KCNQ2 triggers intrinsic neuronal hyperexcitability in ALS/FTD.Nature neuroscience · 2025Article
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- Calcium-sensing receptor regulates Kv7 channels via GBritish journal of pharmacology · 2024Article
- Glycine-induced activation of GPR158 increases the intrinsic excitability of medium spiny neurons in the nucleus accumbens.Cellular and molecular life sciences : CMLS · 2024Article
- Effect of a sensing charge mutation on the deactivation of KV7.2 channels.The Journal of general physiology · 2024Article
- Neuron-oligodendrocyte potassium shuttling at nodes of Ranvier protects against inflammatory demyelination.The Journal of clinical investigation · 2023Article
- Upregulation of astroglial connexin 30 impairs hippocampal synaptic activity and recognition memory.PLoS biology · 2023Article
- Developmental and epileptic encephalopathies: from genetic heterogeneity to phenotypic continuum.Physiological reviews · 2023Review
- Clinical analysis and functional characterization of KCNQ2-related developmental and epileptic encephalopathy.Frontiers in molecular neuroscience · 2023Article
- Mouse models of Kcnq2 dysfunction.Epilepsia · 2022Review
- Tau isoform-specific enhancement of L-type calcium current and augmentation of afterhyperpolarization in rat hippocampal neurons.Scientific reports · 2022Article
- Neuronal KCNQ2/3 channels are recruited to lipid raft microdomains by palmitoylation of BACE1.The Journal of general physiology · 2022Article
- Homeostatic regulation of extracellular signal-regulated kinase 1/2 activity and axonal KFrontiers in cellular neuroscience · 2022Article
- Excitatory and inhibitory hippocampal neurons differ in their homeostatic adaptation to chronic M-channel modulation.Frontiers in molecular neuroscience · 2022Article
- Heterozygous Deletion of Epilepsy GeneFrontiers in behavioral neuroscience · 2022Article
- Spontaneous seizure and memory loss in mice expressing an epileptic encephalopathy variant in the calmodulin-binding domain of KProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Posttranscriptional modulation of KCNQ2 gene expression by the miR-106b microRNA family.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Place fields of single spikes in hippocampus involve Kcnq3 channel-dependent entrainment of complex spike bursts.Nature communications · 2021Article
- CRISPR knockdown of Kcnq3 attenuates the M-current and increases excitability of NPY/AgRP neurons to alter energy balance.Molecular metabolism · 2021Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Benign familial neonatal convulsion (BNFC) is a neurological disorder caused by mutations in the potassium channel genes KCNQ2 and KCNQ3, which are thought to contribute to the medium afterhyperpolarization (mAHP). Despite their importance in normal brain function, it is unknown whether they invariably function as heteromeric complexes. Here, we examined the contribution of KCNQ3 and KCNQ2 in mediating the apamin-insensitive mAHP current (ImAHP) in hippocampus. The ImAHP was not impaired in CA1 pyramidal neurons from mice genetically deficient for either KCNQ3 or KCNQ2 but was reduced approximately 50% in dentate granule cells. While recording from KCNQ-deficient mice, we observed that the calcium-activated slow afterhyperpolarization current (IsAHP) was also reduced in dentate granule cells, suggesting that KCNQ channels might also contribute to this potassium current whose molecular identity is unknown. Further pharmacological and molecular experiments manipulating KCNQ channels provided evidence in support of this possibility. Together our data suggest that multiple KCNQ subunit compositions can mediate the ImAHP, and that the very same subunits may also contribute to the IsAHP. We also present data suggesting that the neuronal calcium sensor protein hippocalcin may allow for these dual signaling processes.
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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.