ArticleNature neuroscience2009
Na+-activated K+ channels express a large delayed outward current in neurons during normal physiology.
Article in Nature neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 118 citations in OpenAlex.
- Unraveling the mechanisms of slack channel mutations in epileptic disorders.Acta epileptologica · 2026Review
- A scaffold attachment factor PHM-2 regulates synaptic transmission through SLO-2 potassium channel in C. elegans.PLoS genetics · 2026Article
- A scaffold attachment factor PHM-2 regulates synaptic transmission through SLO-2 potassium channel inbioRxiv : the preprint server for biology · 2025Article
- Ion Channels in Odor Information Processing of Neural Circuits of the Vertebrate Olfactory Bulb.International journal of molecular sciences · 2024Review
- Heterozygous expression of aeLife · 2024Article
- Heterozygous expression of abioRxiv : the preprint server for biology · 2024Article
- 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
- Distinct Features of Interictal Activity Predict Seizure Localization and Burden in a Mouse Model of Childhood Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Regulation of Neurotransmitter Release by KAdvances in neurobiology · 2023Article
- Review
- Double-edged Role of KCurrent neuropharmacology · 2022Review
- Article
- Slo2/KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- 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
- Sodium sensitivity of KJournal of neurophysiology · 2021Article
- Functional Coupling of Slack Channels and P2X3 Receptors Contributes to Neuropathic Pain Processing.International journal of molecular sciences · 2021Article
- The Functional Properties, Physiological Roles, Channelopathy and Pharmacological Characteristics of the Slack (KCNT1) Channel.Advances in experimental medicine and biology · 2021Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
One of the largest components of the delayed outward current that is active under physiological conditions in many mammalian neurons, such as medium spiny neurons of the striatum and tufted-mitral cells of the olfactory bulb, has gone unnoticed and is the result of a Na(+)-activated K(+) current. Previous studies of K(+) currents in mammalian neurons may have overlooked this large outward component because the sodium channel blocker tetrodotoxin (TTX) is typically used in such studies. We found that TTX also eliminated this delayed outward component in rat neurons as a secondary consequence. Unexpectedly, we found that the activity of a persistent inward sodium current (persistent I(Na)) is highly effective at activating this large Na(+)-dependent (TTX sensitive) delayed outward current. Using siRNA techniques, we identified SLO2.2 channels as being carriers of this delayed outward current. These findings have far reaching implications for many aspects of cellular and systems neuroscience, as well as clinical neurology and pharmacology.
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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.