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.
Model Type: Neuron or other electrically excitable cell; Synapse
Region(s) or Organism(s): Hippocampus
Cell Type(s): Hippocampus CA1 pyramidal GLU cell
Currents: I Na,t; I A; I K; I M; I h; I Calcium; I_AHP
Receptors: AMPA
Transmitters: Glutamate
Model Concept(s): Synaptic Plasticity; Short-term Synaptic Plasticity; Facilitation; Depression; Synaptic Integration; Aging/Alzheimer`s
Simulation Environment: NEURON
Implementer(s): Bianchi, Daniela [danielabianchi12 -at- gmail.com]; Romani, Armando [romani.armando -at- gmail.com]
References:
Romani A et al. (2013). Computational modeling of the effects of amyloid-beta on release probability at hippocampal synapses. Frontiers in computational neuroscience. 7 [PubMed]