ArticleInternational journal of molecular sciences2021
A Mechanistic Model of NMDA and AMPA Receptor-Mediated Synaptic Transmission in Individual Hippocampal CA3-CA1 Synapses: A Computational Multiscale Approach.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Studying Synchronization of Neural Oscillators through NMDA-AMPA Receptor interactions.Chaos, solitons, and fractals · 2026Article
- Designing Neural Dynamics: From Digital Twin Modeling to Regeneration.International journal of molecular sciences · 2025Review
- Computational Modeling of Extrasynaptic NMDA Receptors: Insights into Dendritic Signal Amplification Mechanisms.International journal of molecular sciences · 2024Article
- Short-term Hebbian learning can implement transformer-like attention.PLoS computational biology · 2024Article
- AI-based identification of therapeutic agents targeting GPCRs: introducing ligand type classifiers and systems biology.Chemical science · 2023Article
- Membrane Proteins: Structure, Function and Motion.International journal of molecular sciences · 2022Article
- Postsynaptic Proteins at Excitatory Synapses in the Brain-Relationship with Depressive Disorders.International journal of molecular sciences · 2022Review
- Bridging Hierarchies in Multi-Scale Models of Neural Systems: Look-Up Tables Enable Computationally Efficient Simulations of Non-linear Synaptic Dynamics.Frontiers in computational neuroscience · 2021Article
- Molecular sabotage of hippocampal synaptic plasticity by amyloid-β in Alzheimer's disease: A narrative review.Journal of Alzheimer's disease reportsReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inside hippocampal circuits, neuroplasticity events that individual cells may undergo during synaptic transmissions occur in the form of Long-Term Potentiation (LTP) and Long-Term Depression (LTD). The high density of NMDA receptors expressed on the surface of the dendritic CA1 spines confers to hippocampal CA3-CA1 synapses the ability to easily undergo NMDA-mediated LTP and LTD, which is essential for some forms of explicit learning in mammals. Providing a comprehensive kinetic model that can be used for running computer simulations of the synaptic transmission process is currently a major challenge. Here, we propose a compartmentalized kinetic model for CA3-CA1 synaptic transmission. Our major goal was to tune our model in order to predict the functional impact caused by disease associated variants of NMDA receptors related to severe cognitive impairment. Indeed, for variants Glu413Gly and Cys461Phe, our model predicts negative shifts in the glutamate affinity and changes in the kinetic behavior, consistent with experimental data. These results point to the predictive power of this multiscale viewpoint, which aims to integrate the quantitative kinetic description of large interaction networks typical of system biology approaches with a focus on the quality of a few, key, molecular interactions typical of structural biology ones.
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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.