Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

The synaptic-tagging-and-capture (STC) hypothesis formulates that at each synapse the concurrence of a tag with protein synthesis yields the maintenance of changes induced by synaptic plasticity. This hypothesis provides a biological principle underlying the synaptic consolidation of memories that is not verified for recurrent neural circuits. We developed a theoretical model integrating the mechanisms underlying the STC hypothesis with calcium-based synaptic plasticity in a recurrent spiking neural network. In the model, calcium-based synaptic plasticity yields the formation of strongly interconnected cell assemblies encoding memories, followed by consolidation through the STC mechanisms. Furthermore, we show for the first time that STC mechanisms modify the storage of memories such that after several hours memory recall is significantly improved. We identify two contributing processes: a merely time-dependent passive improvement, and an active improvement during recall. The described characteristics can provide a new principle for storing information in biological and artificial neural circuits. Luboeinski and Tetzlaff develop a theoretical model, which integrates mechanisms underlying the synaptic-tagging-and-capture (STC) hypothesis with calcium-based synaptic plasticity in a recurrent spiking neural network, to describe consolidation of memory representations. They show that STC mechanisms cause improved memory recall, which may assist the understanding of storing information in biological and artificial neural circuits.

Automated summary

The STC hypothesis suggests that a co-occurrence of a tag with protein synthesis at each synapse maintains changes from synaptic plasticity, which, when integrated with calcium-based synaptic plasticity in a theoretical model, leads to the consolidation of memories and improved memory recall.