ArticleNature communications2016
Action potential broadening in a presynaptic channelopathy.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
44 citing papers in PubMed, 77 citations in OpenAlex.
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- Desflurane improves electrical activity of neurons and alleviates oxygen-glucose deprivation-induced neuronal injury by activating the Kcna1-dependent Kv1.1 channel.Experimental brain research · 2024Article
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- KCND2: A prognostic biomarker and regulator of immune function in gastric cancer.Cancer medicine · 2023Article
- Basket to Purkinje Cell Inhibitory Ephaptic Coupling Is Abolished in Episodic Ataxia Type 1.Cells · 2023Article
- What Is the Role of Norepinephrine in Cerebellar Modulation and Stress-Induced Episodic Ataxia?Neurology · 2023Article
- KCa1.1 channels contribute to optogenetically driven post-stimulation silencing in cerebellar molecular layer interneurons.The Journal of general physiology · 2023Article
- The computational power of the human brain.Frontiers in cellular neuroscience · 2023Review
- 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
- Ion Channel Gene Mutations Causing Skeletal Muscle Disorders: Pathomechanisms and Opportunities for Therapy.Cells · 2021Review
- A forward genetic screen identifies Dolk as a regulator of startle magnitude through the potassium channel subunit Kv1.1.PLoS genetics · 2021Article
- Functional Differences Between Two Kv1.1 RNA Editing Isoforms: a Comparative Study on Neuronal Overexpression in Mouse Prefrontal Cortex.Molecular neurobiology · 2021Article
- Chronic nicotine impairs sparse motor learning via striatal fast-spiking parvalbumin interneurons.Addiction biology · 2021Article
- Musculoskeletal Features without Ataxia Associated with a Novel de novo Mutation inBiomedicines · 2021Article
- Large, Stable Spikes Exhibit Differential Broadening in Excitatory and Inhibitory Neocortical Boutons.Cell reports · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Brain development and interictal function are unaffected in many paroxysmal neurological channelopathies, possibly explained by homoeostatic plasticity of synaptic transmission. Episodic ataxia type 1 is caused by missense mutations of the potassium channel Kv1.1, which is abundantly expressed in the terminals of cerebellar basket cells. Presynaptic action potentials of small inhibitory terminals have not been characterized, and it is not known whether developmental plasticity compensates for the effects of Kv1.1 dysfunction. Here we use visually targeted patch-clamp recordings from basket cell terminals of mice harbouring an ataxia-associated mutation and their wild-type littermates. Presynaptic spikes are followed by a pronounced afterdepolarization, and are broadened by pharmacological blockade of Kv1.1 or by a dominant ataxia-associated mutation. Somatic recordings fail to detect such changes. Spike broadening leads to increased Ca(2+) influx and GABA release, and decreased spontaneous Purkinje cell firing. We find no evidence for developmental compensation for inherited Kv1.1 dysfunction.
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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.