ArticleThe Journal of physiology2007
Sodium-dependent potassium channels of a Slack-like subtype contribute to the slow afterhyperpolarization in lamprey spinal neurons.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 95 citations in OpenAlex.
- Reductionist modeling of calcium-dependent dynamics in recurrent neural networks.Frontiers in computational neuroscience · 2025Article
- Disease-causing Slack potassium channel mutations produce opposite effects on excitability of excitatory and inhibitory neurons.Cell reports · 2024Article
- Coupling of Slack and NaeLife · 2024Article
- Slack KCommunications biology · 2023Article
- An in silico and in vitro human neuronal network model reveals cellular mechanisms beyond NaStem cell reports · 2023Article
- KNeurobiology of disease · 2022Article
- The Slack Channel Deletion Causes Mechanical Pain Hypersensitivity in Mice.Frontiers in molecular neuroscience · 2022Article
- Double-edged Role of KCurrent neuropharmacology · 2022Review
- A Role for Transmembrane Protein 16C/Slack Impairment in Excitatory Nociceptive Synaptic Plasticity in the Pathogenesis of Remifentanil-induced Hyperalgesia in Rats.Neuroscience bulletin · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- The Functional Properties, Physiological Roles, Channelopathy and Pharmacological Characteristics of the Slack (KCNT1) Channel.Advances in experimental medicine and biology · 2021Review
- Reduced GABAergic Neuron Excitability, Altered Synaptic Connectivity, and Seizures in a KCNT1 Gain-of-Function Mouse Model of Childhood Epilepsy.Cell reports · 2020Article
- Genomic discovery of ion channel genes in the central nervous system of the lamprey Petromyzon marinus.Marine genomics · 2019Article
- Differential contributions of CaHippocampus · 2018Article
- No fuzzy space for intracellular NaThe Journal of general physiology · 2017Article
- Differential distribution of the sodium-activated potassium channels slick and slack in mouse brain.The Journal of comparative neurology · 2016Article
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- Slack channels expressed in sensory neurons control neuropathic pain in mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The slow afterhyperpolarization (sAHP) following the action potential is the main determinant of spike frequency regulation. The sAHP after single action potentials in neurons of the lamprey locomotor network is largely due to calcium-dependent K+channels (80%), activated by calcium entering the cell during the spike. The residual (20%) component becomes prominent during high level activity (50% of the sAHP). It is not Ca2+ dependent, has a reversal potential like that of potassium, and is not affected by chloride injection. It is not due to rapid activation of Na+/K+-ATPase. This non-KCa-sAHP is reduced markedly in amplitude when sodium ions are replaced by lithium ions, and is thus sodium dependent. Quinidine also blocks this sAHP component, further indicating an involvement of sodium-dependent potassium channels (KNa). Modulators tested do not influence the KNa-sAHP amplitude. Immunofluorescence labelling with an anti-Slack antibody revealed distinct immunoreactivity of medium-sized and large neurons in the grey matter of the lamprey spinal cord, suggesting the presence of a Slack-like subtype of KNa channel. The results strongly indicate that a KNa potassium current contributes importantly to the sAHP and thereby to neuronal frequency regulation during high level burst activity as during locomotion. This is, to our knowledge, the first demonstration of a functional role for the Slack gene in contributing to the slow AHP.
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