ArticlePLoS computational biology2017
β-adrenergic signaling broadly contributes to LTP induction.
Article in PLoS computational biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 33 citations in OpenAlex.
- Calmodulin controls spatial and temporal specificity of calcium-induced calcium release.PLoS computational biology · 2026Article
- Pre- and Post-synaptic Mechanisms of Neuronal Inhibition Assessed Through Biochemically Detailed Modeling of GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Fitting and comparison of calcium-calmodulin kinetic schemes to a common data set using non-linear mixed effects modelling.PloS one · 2025Article
- β-adrenergic receptor-induced E-S potentiation in the dorsal and ventral hippocampus.Frontiers in synaptic neuroscience · 2024Article
- Making time and space for calcium control of neuron activity.Current opinion in neurobiology · 2023Review
- Muscarinic acetylcholine receptor-dependent and NMDA receptor-dependent LTP and LTD share the common AMPAR trafficking pathway.iScience · 2023Article
- Adaptive control of synaptic plasticity integrates micro- and macroscopic network function.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Norepinephrine, beyond the Synapse: Coordinating Epigenetic Codes for Memory.International journal of molecular sciences · 2022Review
- Computational investigation of the dynamic control of cAMP signaling by PDE4 isoform types.Biophysical journal · 2022Article
- An emerging role for microglia in stress-effects on memory.The European journal of neuroscience · 2022Review
- A computational model of dopaminergic modulation of hippocampal Schaffer collateral-CA1 long-term plasticity.Journal of computational neuroscience · 2022Article
- Review
- Temporal pattern and synergy influence activity of ERK signaling pathways during L-LTP induction.eLife · 2021Article
- Noradrenergic Enhancement of Motor Learning, Attention, and Working Memory in Humans.The international journal of neuropsychopharmacology · 2021Article
- Roles of palmitoylation in structural long-term synaptic plasticity.Molecular brain · 2021Review
- A Multisubcellular Compartment Model of AMPA Receptor Trafficking for Neuromodulation of Hebbian Synaptic Plasticity.Frontiers in synaptic neuroscience · 2021Article
- Article
- From membrane receptors to protein synthesis and actin cytoskeleton: Mechanisms underlying long lasting forms of synaptic plasticity.Seminars in cell & developmental biology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Long-lasting forms of long-term potentiation (LTP) represent one of the major cellular mechanisms underlying learning and memory. One of the fundamental questions in the field of LTP is why different molecules are critical for long-lasting forms of LTP induced by diverse experimental protocols. Further complexity stems from spatial aspects of signaling networks, such that some molecules function in the dendrite and some are critical in the spine. We investigated whether the diverse experimental evidence can be unified by creating a spatial, mechanistic model of multiple signaling pathways in hippocampal CA1 neurons. Our results show that the combination of activity of several key kinases can predict the occurrence of long-lasting forms of LTP for multiple experimental protocols. Specifically Ca2+/calmodulin activated kinase II, protein kinase A and exchange protein activated by cAMP (Epac) together predict the occurrence of LTP in response to strong stimulation (multiple trains of 100 Hz) or weak stimulation augmented by isoproterenol. Furthermore, our analysis suggests that activation of the β-adrenergic receptor either via canonical (Gs-coupled) or non-canonical (Gi-coupled) pathways underpins most forms of long-lasting LTP. Simulations make the experimentally testable prediction that a complete antagonist of the β-adrenergic receptor will likely block long-lasting LTP in response to strong stimulation. Collectively these results suggest that converging molecular mechanisms allow CA1 neurons to flexibly utilize signaling mechanisms best tuned to temporal pattern of synaptic input to achieve long-lasting LTP and memory storage.
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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.