ArticleFrontiers in computational neuroscience2013
Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses.
Article in Frontiers in computational neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Article
- Altered synaptic plasticity at hippocampal CA1-CA3 synapses in Alzheimer's disease: integration of amyloid precursor protein intracellular domain and amyloid beta effects into computational models.Frontiers in computational neuroscience · 2023Article
- The Involvement of Insulin-Like Growth Factor 1 and Nerve Growth Factor in Alzheimer's Disease-Like Pathology and Survival Role of the Mix of Embryonic Proteoglycans: Electrophysiological Fingerprint, Structural Changes and Regulatory Effects on Neurotrophins.International journal of molecular sciences · 2021Article
- Modeling Neurotransmission: Computational Tools to Investigate Neurological Disorders.International journal of molecular sciences · 2021Review
- Bridging Scales in Alzheimer's Disease: Biological Framework for Brain Simulation With The Virtual Brain.Frontiers in neuroinformatics · 2021Review
- The Human Body as a Super Network: Digital Methods to Analyze the Propagation of Aging.Frontiers in aging neuroscience · 2020Article
- Model-Based Inference of Synaptic Transmission.Frontiers in synaptic neuroscience · 2019Review
- Computational modeling and biomarker studies of pharmacological treatment of Alzheimer's disease (Review).Molecular medicine reports · 2018Review
- Synapses in neurodegenerative diseases.BMB reports · 2017Review
- The Impact of Mathematical Modeling in Understanding the Mechanisms Underlying Neurodegeneration: Evolving Dimensions and Future Directions.CPT: pharmacometrics & systems pharmacology · 2017Review
- Emulating short-term synaptic dynamics with memristive devices.Scientific reports · 2016Article
- Capturing intracellular CaDrug discovery today. Disease models · 2016Article
- Article
- Adaptation of short-term plasticity parameters via error-driven learning may explain the correlation between activity-dependent synaptic properties, connectivity motifs and target specificity.Frontiers in computational neuroscience · 2014Article
- Probabilistic inference of short-term synaptic plasticity in neocortical microcircuits.Frontiers in computational neuroscience · 2013Article
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Authors and funding
7 authors.
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Abstract
The role of amyloid beta (Aβ) in brain function and in the pathogenesis of Alzheimer's disease (AD) remains elusive. Recent publications reported that an increase in Aβ concentration perturbs pre-synaptic release in hippocampal neurons. In particular, it was shown in vitro that Aβ is an endogenous regulator of synaptic transmission at the CA3-CA1 synapse, enhancing its release probability. How this synaptic modulator influences neuronal output during physiological stimulation patterns, such as those elicited in vivo, is still unknown. Using a realistic model of hippocampal CA1 pyramidal neurons, we first implemented this Aβ-induced enhancement of release probability and validated the model by reproducing the experimental findings. We then demonstrated that this synaptic modification can significantly alter synaptic integration properties in a wide range of physiologically relevant input frequencies (from 5 to 200 Hz). Finally, we used natural input patterns, obtained from CA3 pyramidal neurons in vivo during free exploration of rats in an open field, to investigate the effects of enhanced Aβ on synaptic release under physiological conditions. The model shows that the CA1 neuronal response to these natural patterns is altered in the increased-Aβ condition, especially for frequencies in the theta and gamma ranges. These results suggest that the perturbation of release probability induced by increased Aβ can significantly alter the spike probability of CA1 pyramidal neurons and thus contribute to abnormal hippocampal function during AD.
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