Synaptic scaling balances learning in a spiking model of neocortex (Rowan & Neymotin 2013)


Learning in the brain requires complementary mechanisms: potentiation and activity-dependent homeostatic scaling. We introduce synaptic scaling to a biologically-realistic spiking model of neocortex which can learn changes in oscillatory rhythms using STDP, and show that scaling is necessary to balance both positive and negative changes in input from potentiation and atrophy. We discuss some of the issues that arise when considering synaptic scaling in such a model, and show that scaling regulates activity whilst allowing learning to remain unaltered.

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; Abstract integrate-and-fire adaptive exponential (AdEx) neuron

Receptors: GabaA; AMPA; NMDA

Transmitters: Gaba; Glutamate

Model Concept(s): Synaptic Plasticity; Long-term Synaptic Plasticity; Learning; STDP; 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. (2013). Synaptic Scaling Balances Learning in a Spiking Model of Neocortex Adaptive and Natural Computing Algorithms. 7824


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