Abstract
Synaptic plasticity, the putative basis of learning and memory formation, manifests in various forms and across different timescales. Here we show that the interaction of Hebbian homosynaptic plasticity with rapid non-Hebbian heterosynaptic plasticity is, when complemented with slower homeostatic changes and consolidation, sufficient for assembly formation and memory recall in a spiking recurrent network model of excitatory and inhibitory neurons. In the model, assemblies were formed during repeated sensory stimulation and characterized by strong recurrent excitatory connections. Even days after formation, and despite ongoing network activity and synaptic plasticity, memories could be recalled through selective delay activity following the brief stimulation of a subset of assembly neurons. Blocking any component of plasticity prevented stable functioning as a memory network. Our modelling results suggest that the diversity of plasticity phenomena in the brain is orchestrated towards achieving common functional goals.
Highlights
Synaptic plasticity, the putative basis of learning and memory formation, manifests in various forms and across different timescales
They are contrasted by rapidly ‘induced’ plasticity caused on the one hand by typical plasticity protocols, for example, for the induction of long-term potentiation (LTP) and depression (LTD), and on the other hand by fast compensatory mechanisms that include non-Hebbian forms of plasticity
We show that the concerted action of local homosynaptic, heterosynaptic and transmitter-triggered forms of plasticity at excitatory synapses leads to stable assembly formation and recall in recurrent networks of spiking neurons
Summary
The putative basis of learning and memory formation, manifests in various forms and across different timescales. We show that the interaction of Hebbian homosynaptic plasticity with rapid non-Hebbian heterosynaptic plasticity is, when complemented with slower homeostatic changes and consolidation, sufficient for assembly formation and memory recall in a spiking recurrent network model of excitatory and inhibitory neurons. We refer to slow compensatory processes that act on a timescale above 10 min as ‘homeostatic’ They are contrasted by rapidly ‘induced’ plasticity caused on the one hand by typical plasticity protocols (lasting a few seconds to tens of seconds), for example, for the induction of long-term potentiation (LTP) and depression (LTD), and on the other hand by fast compensatory mechanisms that include non-Hebbian forms of plasticity. We show that the concerted action of local homosynaptic, heterosynaptic and transmitter-triggered forms of plasticity at excitatory synapses leads to stable assembly formation and recall in recurrent networks of spiking neurons
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