"... As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. ... The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, ... Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. ... "
Model Type: Realistic Network
Region(s) or Organism(s): Neocortex
Cell Type(s): Neocortex L5/6 pyramidal GLU cell; Neocortex L2/3 pyramidal GLU cell; Neocortex V1 interneuron basket PV GABA cell; Neocortex fast spiking (FS) interneuron; Neocortex spiny stellate cell; Neocortex spiking regular (RS) neuron; Neocortex spiking low threshold (LTS) neuron
Model Concept(s): Long-term Synaptic Plasticity; Aging/Alzheimer`s; Deep brain stimulation; Homeostasis
Simulation Environment: NEURON; Python
Implementer(s): Lytton, William [bill.lytton at downstate.edu]; Neymotin, Sam [Samuel.Neymotin at nki.rfmh.org]; Rowan, Mark [m.s.rowan at cs.bham.ac.uk]
References:
Rowan MS, Neymotin SA, Lytton WW. (2014). Electrostimulation to reduce synaptic scaling driven progression of Alzheimer's disease. Frontiers in computational neuroscience. 8 [PubMed]