ArticleProceedings of the National Academy of Sciences of the United States of America2017
Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Membrane potential states gate synaptic consolidation in human neocortical tissue.Nature communications · 2024Article
- Beyond a Transmission Cable-New Technologies to Reveal the Richness in Axonal Electrophysiology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- Interfacing Aptamer-Modified Nanopipettes with Neuronal Media andACS measurement science au · 2024Article
- Basket to Purkinje Cell Inhibitory Ephaptic Coupling Is Abolished in Episodic Ataxia Type 1.Cells · 2023Article
- The computational power of the human brain.Frontiers in cellular neuroscience · 2023Review
- On-demand cell-autonomous gene therapy for brain circuit disorders.Science (New York, N.Y.) · 2022Article
- Homeostatic regulation of axonal Kv1.1 channels accounts for both synaptic and intrinsic modifications in the hippocampal CA3 circuit.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization.Brain : a journal of neurology · 2021Article
- Scanning Ion Conductance Microscopy.Chemical reviews · 2021Review
- Voltage-Gated Potassium Channels Ensure Action Potential Shape Fidelity in Distal Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Subcellular patch-clamp techniques for single-bouton stimulation and simultaneous pre- and postsynaptic recording at cortical synapses.Nature protocols · 2021Article
- Large, Stable Spikes Exhibit Differential Broadening in Excitatory and Inhibitory Neocortical Boutons.Cell reports · 2021Article
- The potassium channel subunit KProceedings of the National Academy of Sciences of the United States of America · 2020Article
- In vivo CRISPRa decreases seizures and rescues cognitive deficits in a rodent model of epilepsy.Brain : a journal of neurology · 2020Article
- Subcellular control of membrane excitability in the axon.Current opinion in neurobiology · 2019Review
- Past and Future of Analog-Digital Modulation of Synaptic Transmission.Frontiers in cellular neuroscience · 2019Review
- Genetically Encoded Voltage Indicators Are Illuminating Subcellular Physiology of the Axon.Frontiers in cellular neuroscience · 2019Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Although action potentials propagate along axons in an all-or-none manner, subthreshold membrane potential fluctuations at the soma affect neurotransmitter release from synaptic boutons. An important mechanism underlying analog-digital modulation is depolarization-mediated inactivation of presynaptic Kv1-family potassium channels, leading to action potential broadening and increased calcium influx. Previous studies have relied heavily on recordings from blebs formed after axon transection, which may exaggerate the passive propagation of somatic depolarization. We recorded instead from small boutons supplied by intact axons identified with scanning ion conductance microscopy in primary hippocampal cultures and asked how distinct potassium channels interact in determining the basal spike width and its modulation by subthreshold somatic depolarization. Pharmacological or genetic deletion of Kv1.1 broadened presynaptic spikes without preventing further prolongation by brief depolarizing somatic prepulses. A heterozygous mouse model of episodic ataxia type 1 harboring a dominant Kv1.1 mutation had a similar broadening effect on basal spike shape as deletion of Kv1.1; however, spike modulation by somatic prepulses was abolished. These results argue that the Kv1.1 subunit is not necessary for subthreshold modulation of spike width. However, a disease-associated mutant subunit prevents the interplay of analog and digital transmission, possibly by disrupting the normal stoichiometry of presynaptic potassium channels.
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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.