ArticleNature communications2016
Coordinated activation of distinct Ca(2+) sources and metabotropic glutamate receptors encodes Hebbian synaptic plasticity.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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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
41 citing papers in PubMed, 77 citations in OpenAlex.
- The how and why for multiple forms of hippocampal LTP.Frontiers in synaptic neuroscience · 2026Review
- Metabotropic Glutamate Receptor-Dependent Synaptic Plasticity in Age-Related Neurodegenerative Disorders.Neural plasticity · 2026Review
- A generalized mathematical framework for the calcium control hypothesis describes weight-dependent synaptic plasticity.Journal of computational neuroscience · 2025Article
- Discovery of FO-4-15, a novel 1,2,4-oxadiazole derivative, ameliorates cognitive impairments in 3×Tg mice by activating the mGluR1/CaMKIIα pathway.Acta pharmacologica Sinica · 2025Article
- The calcitron: A simple neuron model that implements many learning rules via the calcium control hypothesis.PLoS computational biology · 2025Article
- Promiscuous involvement of metabotropic glutamate receptors in the storage ofPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
- The small conductance CaNeuropharmacology · 2024Article
- Calcium- and calmodulin-dependent inhibition of NMDA receptor currents.Biophysical journal · 2024Review
- BK channels sustain neuronal CaCellular and molecular life sciences : CMLS · 2023Article
- A stochastic model of hippocampal synaptic plasticity with geometrical readout of enzyme dynamics.eLife · 2023Article
- Asymmetric Voltage Attenuation in Dendrites Can Enable Hierarchical Heterosynaptic Plasticity.eNeuro · 2023Article
- αeLife · 2023Article
- Control systems theory revisited: new insights on the brain clocks of time-to-action.Frontiers in neuroscience · 2023Article
- Spike-timing-dependent plasticity rewards synchrony rather than causality.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Reduced expression of the psychiatric risk gene DLG2 (PSD93) impairs hippocampal synaptic integration and plasticity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Article
- Neurotrophin receptor activation rescues cognitive and synaptic abnormalities caused by hemizygosity of the psychiatric risk gene Cacna1c.Molecular psychiatry · 2021Article
- SK2 channel regulation of neuronal excitability, synaptic transmission, and brain rhythmic activity in health and diseases.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Interneuron-specific plasticity at parvalbumin and somatostatin inhibitory synapses onto CA1 pyramidal neurons shapes hippocampal output.Nature communications · 2020Article
- Synaptic Plasticity Depends on the Fine-Scale Input Pattern in Thin Dendrites of CA1 Pyramidal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Spatial Coupling Tunes NMDA Receptor Responses via CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
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5 authors at 1 institution in 1 country.
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Abstract
At glutamatergic synapses, induction of associative synaptic plasticity requires time-correlated presynaptic and postsynaptic spikes to activate postsynaptic NMDA receptors (NMDARs). The magnitudes of the ensuing Ca2+ transients within dendritic spines are thought to determine the amplitude and direction of synaptic change. In contrast, we show that at mature hippocampal Schaffer collateral synapses the magnitudes of Ca2+ transients during plasticity induction do not match this rule. Indeed, LTP induced by time-correlated pre- and postsynaptic spikes instead requires the sequential activation of NMDARs followed by voltage-sensitive Ca2+ channels within dendritic spines. Furthermore, LTP requires inhibition of SK channels by mGluR1, which removes a negative feedback loop that constitutively regulates NMDARs. Therefore, rather than being controlled simply by the magnitude of the postsynaptic calcium rise, LTP induction requires the coordinated activation of distinct sources of Ca2+ and mGluR1-dependent facilitation of NMDAR function.
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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.