ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Opposite regulation of Slick and Slack K+ channels by neuromodulators.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Intellectual Disability and Potassium Channelopathies: A Systematic Review.Frontiers in genetics · 2020Pooled it
- SLO2.1/NALCN Functional Complex Activity in Mouse Myometrial Smooth Muscle Cells During Pregnancy.Journal of cellular physiology · 2025Article
- Decoding bee cleptoparasitism through comparative transcriptomics of Coelioxoides waltheriae and its host Tetrapedia diversipes.Scientific reports · 2024Article
- Case Report: Targeted treatment by fluoxetine/norfluoxetine of aFrontiers in pharmacology · 2024Article
- SLO3: A Conserved Regulator of Sperm Membrane Potential.International journal of molecular sciences · 2023Review
- BK channels of five different subunit combinations underlie the de novo KCNMA1 G375R channelopathy.The Journal of general physiology · 2023Article
- Article
- A KCNC1 mutation in epilepsy of infancy with focal migrating seizures produces functional channels that fail to be regulated by PKC phosphorylation.Journal of neurophysiology · 2021Article
- The Functional Properties, Physiological Roles, Channelopathy and Pharmacological Characteristics of the Slack (KCNT1) Channel.Advances in experimental medicine and biology · 2021Review
- Modulation of Neuronal Potassium Channels During Auditory Processing.Frontiers in neuroscience · 2021Review
- Impaired motor skill learning and altered seizure susceptibility in mice with loss or gain of function of the Kcnt1 gene encoding Slack (KScientific reports · 2020Article
- The Epilepsy of Infancy With Migrating Focal Seizures: Identification ofFrontiers in cellular neuroscience · 2020Article
- Phactr1 regulates Slack (KCNT1) channels via protein phosphatase 1 (PP1).FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Sodium-activated potassium channels moderate excitability in vascular smooth muscle.The Journal of physiology · 2019Article
- An Epilepsy-Associated KCNT1 Mutation Enhances Excitability of Human iPSC-Derived Neurons by Increasing Slack KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Genome wide association study on feed conversion ratio using imputed sequence data in chickens.Asian-Australasian journal of animal sciences · 2019Article
- Oxytocin can regulate myometrial smooth muscle excitability by inhibiting the NaThe Journal of physiology · 2019Article
- Quinidine Therapy for Lennox-Gastaut Syndrome WithFrontiers in neurology · 2019Article
- Metabolic and molecular framework for the enhancement of endurance by intermittent food deprivation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Ion Channels in Genetic Epilepsy: From Genes and Mechanisms to Disease-Targeted Therapies.Pharmacological reviews · 2018Review
3 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Slick (Slo2.1) and Slack (Slo2.2) are two novel members of the mammalian Slo potassium channel gene family that may contribute to the resting potentials of cells and control their basal level of excitability. Slo2 channels have sensors that couple channel activity to the intracellular concentrations of Na+ and Cl- ions (Yuan et al., 2003). We now report that activity of both Slo2 channels is controlled by neuromodulators through Galphaq-protein coupled receptors (GqPCRs) (the M1 muscarinic receptor and the mGluR1 metabotropic glutamate receptor). Experiments coexpressing channels and receptors in Xenopus oocytes show that Slo2.1 and Slo2.2 channels are modulated in opposite ways: Slo2.1 is strongly inhibited, whereas Slo2.2 currents are strongly activated through GqPCR stimulation. Differential regulation involves protein kinase C (PKC); application of the PKC activator PMA, to cells expressing channels but not receptors, inhibits Slo2.1 whole-cell currents and increases Slo2.2 currents. Synthesis of a chimera showed that the distal carboxyl region of Slo2.1 controls the sensitivity of Slo2.1 to PMA. Slo2 channels have widespread expression in brain (Bhattacharjee et al., 2002, 2005). Using immunocytochemical techniques, we show coexpression of Slo2 channels with the GqPCRs in cortical and hippocampal brain sections and in cultured hippocampal neurons. The differential control of these novel channels by neurotransmitters may elicit long-lasting increases or decreases in neuronal excitability and, because of their widespread distribution, may provide a mechanism to activate or repress electrical activity in many systems of the brain.
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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.