ArticleThe Journal of physiology2008
Spike Ca2+ influx upmodulates the spike afterdepolarization and bursting via intracellular inhibition of KV7/M channels.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Trial
- Dendritic interaction of timescales in afterdepolarization potentials and nonmonotonic spike-adding.Journal of computational neuroscience · 2026Article
- Biphasic Cholinergic Modulation of Reverberatory Activity in Neuronal Networks.Neuroscience bulletin · 2023Article
- Kcnq2/Kv7.2 controls the threshold and bi-hemispheric symmetry of cortical spreading depolarization.Brain : a journal of neurology · 2021Article
- M-Current Inhibition in Hippocampal Excitatory Neurons Triggers Intrinsic and Synaptic Homeostatic Responses at Different Temporal Scales.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Differential contributions of CaHippocampus · 2018Article
- KThe Journal of physiology · 2017Article
- Learning Universal Computations with Spikes.PLoS computational biology · 2016Article
- Impaired firing properties of dentate granule neurons in an Alzheimer's disease animal model are rescued by PPARγ agonism.Journal of neurophysiology · 2015Article
- Role of small conductance Ca²⁺-activated K⁺ channels in controlling CA1 pyramidal cell excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- A novel phase portrait for neuronal excitability.PloS one · 2012Article
- Muscarinic acetylcholine receptors (mAChRs) in the nervous system: some functions and mechanisms.Journal of molecular neuroscience : MN · 2010Review
- KV7/M channels mediate osmotic modulation of intrinsic neuronal excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Neural KCNQ (Kv7) channels.British journal of pharmacology · 2009Review
- Activity-dependent depression of the spike after-depolarization generates long-lasting intrinsic plasticity in hippocampal CA3 pyramidal neurons.The Journal of physiology · 2009Article
- Nanomedicine: shorting neurons with nanotubes.Nature nanotechnology · 2009Article
- Low expression of Kv7/M channels facilitates intrinsic and network bursting in the developing rat hippocampus.The Journal of physiology · 2008Article
- Homomeric and heteromeric assembly of KCNQ (Kv7) K+ channels assayed by total internal reflection fluorescence/fluorescence resonance energy transfer and patch clamp analysis.The Journal of biological chemistry · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In principal brain neurons, activation of Ca(2+) channels during an action potential, or spike, causes Ca(2+) entry into the cytosol within a millisecond. This in turn causes rapid activation of large conductance Ca(2+)-gated channels, which enhances repolarization and abbreviates the spike. Here we describe another remarkable consequence of spike Ca(2+) entry: enhancement of the spike afterdepolarization. This action is also mediated by intracellular modulation of a particular class of K(+) channels, namely by inhibition of K(V)7 (KCNQ) channels. These channels generate the subthreshold, non-inactivating M-type K(+) current, whose activation curtails the spike afterdepolarization. Inhibition of K(V)7/M by spike Ca(2+) entry allows the spike afterdepolarization to grow and can convert solitary spikes into high-frequency bursts of action potentials. Through this novel intracellular modulatory action, Ca(2+) spike entry regulates the discharge mode and the signalling capacity of principal brain neurons.
Indexed as
Identifiers
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.