ArticlePLoS computational biology2016
Control of Ca2+ Influx and Calmodulin Activation by SK-Channels in Dendritic Spines.
Article in PLoS computational biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 44 citations in OpenAlex.
- GluN2A- and GluN2B-containing pre-synapticPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- Nano-organization of synaptic calcium signaling.Biochemical Society transactions · 2024Review
- Making time and space for calcium control of neuron activity.Current opinion in neurobiology · 2023Review
- A stochastic model of hippocampal synaptic plasticity with geometrical readout of enzyme dynamics.eLife · 2023Article
- Dendritic spine morphology regulates calcium-dependent synaptic weight change.The Journal of general physiology · 2022Article
- Periodicity Pitch Perception Part III: Sensibility and Pachinko Volatility.Frontiers in neuroscience · 2022Article
- APOE4 Affects Basal and NMDAR-Mediated Protein Synthesis in Neurons by Perturbing Calcium Homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Stationary CaBiophysical journal · 2021Article
- Interneuron-specific plasticity at parvalbumin and somatostatin inhibitory synapses onto CA1 pyramidal neurons shapes hippocampal output.Nature communications · 2020Article
- Estrogen Receptor β2 Oversees Germ Cell Maintenance and Gonadal Sex Differentiation in Medaka, Oryzias latipes.Stem cell reports · 2019Article
- Dendritic spine geometry and spine apparatus organization govern the spatiotemporal dynamics of calcium.The Journal of general physiology · 2019Article
- Voltage-Independent SK-Channel Dysfunction Causes Neuronal Hyperexcitability in the Hippocampus ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Biophysical modeling of C. elegans neurons: Single ion currents and whole-cell dynamics of AWCon and RMD.PloS one · 2019Article
- Convergent Metabotropic Signaling Pathways Inhibit SK Channels to Promote Synaptic Plasticity in the Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Extension of Rapid Buffering Approximation to CaBiophysical journal · 2018Article
- Modulation of Spike-Timing Dependent Plasticity: Towards the Inclusion of a Third Factor in Computational Models.Frontiers in computational neuroscience · 2018Review
- A Putative Mechanism of Age-Related Synaptic Dysfunction Based on the Impact of IGF-1 Receptor Signaling on Synaptic CaMKIIα Phosphorylation.Frontiers in neuroanatomy · 2018Article
- Spike Frequency Adaptation in Neurons of the Central Nervous System.Experimental neurobiology · 2017Review
- SK channel subtypes enable parallel optimized coding of behaviorally relevant stimulus attributes: A review.Channels (Austin, Tex.) · 2017Review
- Neuromodulation of the Feedforward Dentate Gyrus-CA3 Microcircuit.Frontiers in synaptic neuroscience · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The key trigger for Hebbian synaptic plasticity is influx of Ca2+ into postsynaptic dendritic spines. The magnitude of [Ca2+] increase caused by NMDA-receptor (NMDAR) and voltage-gated Ca2+ -channel (VGCC) activation is thought to determine both the amplitude and direction of synaptic plasticity by differential activation of Ca2+ -sensitive enzymes such as calmodulin. Ca2+ influx is negatively regulated by Ca2+ -activated K+ channels (SK-channels) which are in turn inhibited by neuromodulators such as acetylcholine. However, the precise mechanisms by which SK-channels control the induction of synaptic plasticity remain unclear. Using a 3-dimensional model of Ca2+ and calmodulin dynamics within an idealised, but biophysically-plausible, dendritic spine, we show that SK-channels regulate calmodulin activation specifically during neuron-firing patterns associated with induction of spike timing-dependent plasticity. SK-channel activation and the subsequent reduction in Ca2+ influx through NMDARs and L-type VGCCs results in an order of magnitude decrease in calmodulin (CaM) activation, providing a mechanism for the effective gating of synaptic plasticity induction. This provides a common mechanism for the regulation of synaptic plasticity by neuromodulators.
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.