ArticleeLife2016
IK1 channels do not contribute to the slow afterhyperpolarization in pyramidal neurons.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 41 citations in OpenAlex.
- IK Channel Confers Fine-tuning of Rod Bipolar Cell Excitation and Synaptic Transmission in the Retina.Function (Oxford, England) · 2025Article
- Challenges in the Therapeutic Targeting of KCa Channels: From Basic Physiology to Clinical Applications.International journal of molecular sciences · 2024Review
- A Pathogenic Missense Mutation in Kainate Receptors Elevates Dendritic Excitability and Synaptic Integration through Dysregulation of SK Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Ion Channel Partnerships: Odd and Not-So-Odd Couples Controlling Neuronal Ion Channel Function.International journal of molecular sciences · 2022Review
- Olfactory rule learning-induced enhancement in intrinsic neuronal excitability is maintained by shutdown of the cholinergic M-current.Frontiers in cellular neuroscience · 2022Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- CaScientific reports · 2020Article
- The role of L-type calcium channels in neuronal excitability and aging.Neurobiology of learning and memory · 2020Review
- Pharmacology of Small- and Intermediate-Conductance Calcium-Activated Potassium Channels.Annual review of pharmacology and toxicology · 2020Review
- Learning and aging affect neuronal excitability and learning.Neurobiology of learning and memory · 2020Review
- Regulation of intrinsic excitability: Roles for learning and memory, aging and Alzheimer's disease, and genetic diversity.Neurobiology of learning and memory · 2019Review
- Differential contributions of CaHippocampus · 2018Article
- KCa3.1 Channel Modulators as Potential Therapeutic Compounds for Glioblastoma.Current neuropharmacology · 2018Article
- Physiological Roles and Therapeutic Potential of CaFrontiers in molecular neuroscience · 2018Review
- Activity-Dependent Facilitation of CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- International Union of Basic and Clinical Pharmacology. C. Nomenclature and Properties of Calcium-Activated and Sodium-Activated Potassium Channels.Pharmacological reviews · 2017Review
- CA1 pyramidal cells have diverse biophysical properties, affected by development, experience, and aging.PeerJ · 2017Article
- Assessing the role of IKCa channels in generating the sAHP of CA1 hippocampal pyramidal cells.Channels (Austin, Tex.) · 2016Article
- KCa3.1 Impairment Is Not Just a Slow Afterthought in Epilepsy.Epilepsy currentsArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
In pyramidal neurons such as hippocampal area CA1 and basolateral amygdala, a slow afterhyperpolarization (sAHP) follows a burst of action potentials, which is a powerful regulator of neuronal excitability. The sAHP amplitude increases with aging and may underlie age related memory decline. The sAHP is due to a Ca(2+)-dependent, voltage-independent K(+) conductance, the molecular identity of which has remained elusive until a recent report suggested the Ca(2+)-activated K(+) channel, IK1 (KCNN4) as the sAHP channel in CA1 pyramidal neurons. The signature pharmacology of IK1, blockade by TRAM-34, was reported for the sAHP and underlying current. We have examined the sAHP and find no evidence that TRAM-34 affects either the current underling the sAHP or excitability of CA1 or basolateral amygdala pyramidal neurons. In addition, CA1 pyramidal neurons from IK1 null mice exhibit a characteristic sAHP current. Our results indicate that IK1 channels do not mediate the sAHP in pyramidal neurons.
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What OpenQuestion holds
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.