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Amyloid-beta effects on release probability and integration at CA3-CA1 synapses (Romani et al. 2013)
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The role of amyloid beta (Aß) in brain function and in the pathogenesis of Alzheimer’s disease remains elusive. Recent publications reported that an increase in Aß concentration perturbs presynaptic release in hippocampal neurons, in particular by increasing release probability of CA3-CA1 synapses. The model predics how this alteration can affect synaptic plasticity and signal integration. The results suggest that the perturbation of release probability induced by increased Aß can significantly alter the spike probability of CA1 pyramidal neurons and thus contribute to abnormal hippocampal function during Alzheimer’s disease.
Romani A, Marchetti C, Bianchi D, Leinekugel X, Poirazi P, Migliore M, Marie H (2013) Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses.
Front Comput Neurosci
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Neuron or other electrically excitable cell;
Hippocampus CA1 pyramidal GLU cell;
Short-term Synaptic Plasticity;
Bianchi, Daniela [danielabianchi12 -at- gmail.com];
Romani, Armando [romani.armando -at- gmail.com];
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Hippocampus CA1 pyramidal GLU cell
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