ArticleBiophysical journal2012
Hippocalcin and KCNQ channels contribute to the kinetics of the slow afterhyperpolarization.
Article in Biophysical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
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- Modeling Time Cell Neuron-Level Dynamics.Computational brain & behavior · 2024Article
- Effect of a sensing charge mutation on the deactivation of KV7.2 channels.The Journal of general physiology · 2024Article
- Benign Hereditary Chorea as a Manifestation of HPCA Mutation.Movement disorders clinical practice · 2023Article
- Genetic Dystonias: Update on Classification and New Genetic Discoveries.Current neurology and neuroscience reports · 2021Review
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Differential contributions of CaHippocampus · 2018Article
- Biophysical and functional characterization of hippocalcin mutants responsible for human dystonia.Human molecular genetics · 2017Article
- Proteome-wide Identification of Novel Ceramide-binding Proteins by Yeast Surface cDNA Display and Deep Sequencing.Molecular & cellular proteomics : MCP · 2016Article
- The Voltage Activation of Cortical KCNQ Channels Depends on Global PIP2 Levels.Biophysical journal · 2016Article
- High-fat diet impairs spatial memory and hippocampal intrinsic excitability and sex-dependently alters circulating insulin and hippocampal insulin sensitivity.Biology of sex differences · 2016Article
- Structure and Calcium Binding Properties of a Neuronal Calcium-Myristoyl Switch Protein, Visinin-Like Protein 3.PloS one · 2016Article
- Mutations in HPCA cause autosomal-recessive primary isolated dystonia.American journal of human genetics · 2015Article
- Homeostasis or channelopathy? Acquired cell type-specific ion channel changes in temporal lobe epilepsy and their antiepileptic potential.Frontiers in physiology · 2015Review
- Transcriptome analyses of inhibitor-treated schistosome females provide evidence for cooperating Src-kinase and TGFβ receptor pathways controlling mitosis and eggshell formation.PLoS pathogens · 2013Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
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Abstract
The calcium-activated slow afterhyperpolarization (sAHP) is a potassium conductance implicated in many physiological functions of the brain including memory, aging, and epilepsy. In large part, the sAHP's importance stems from its exceedingly long-lasting time-course, which integrates action potential-induced calcium signals and allows the sAHP to control neuronal excitability and prevent runaway firing. Despite its role in neuronal physiology, the molecular mechanisms that give rise to its unique kinetics are, to our knowledge, still unknown. Recently, we identified KCNQ channels as a candidate potassium channel family that can contribute to the sAHP. Here, we test whether KCNQ channels shape the sAHP rise and decay kinetics in wild-type mice and mice lacking Hippocalcin, the putative sAHP calcium sensor. Application of retigabine to speed KCNQ channel activation accelerated the rise of the CA3 pyramidal neuron sAHP current in both wild-type and Hippocalcin knockout mice, indicating that the gating of KCNQ channels limits the sAHP activation. Interestingly, we found that the decay of the sAHP was prolonged in Hippocalcin knockout mice, and that the decay was sensitive to retigabine modulation, unlike in wild-type mice. Together, our results demonstrate that sAHP activation in CA3 pyramidal neurons is critically dependent on KCNQ channel kinetics whereas the identity of the sAHP calcium sensor determines whether KCNQ channel kinetics also limit the sAHP decay.
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