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

Abstract

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.

Formation and computational implications of assemblies in neural circuits

“…disinhibition as a gating signal (Froemke et al., 2007; Letzkus et al., 2011) or ‘three‐factor plasticity rules’, where neuromodulators that convey a learning signal can regulate weight change in addition to the pre‐ and postsynaptic activity (Frémaux & Gerstner, 2016). Another mechanism is synaptic tagging and capture, where activity‐dependent synaptic plasticity needs an additional stabilising internal signal to allow persistent connectivity changes (Luboeinski & Tetzlaff, 2021; Redondo & Morris, 2011).…”

Pre- and postsynaptic N-methyl-D-aspartate receptors are required for sequential printing of fear memory engrams

“…With early tagging of neural circuits, 85 , 87 the generation of BLA-mPFC memory engrams 31 , 35 and other brain regions, 83 even in an evolutionarily older brain structure such as the hypothalamus, 72 provide multiple pathways for flexible memory retrieval. 27 , 28 , 35 , 88 These findings prompted us to propose that memory engrams are sequentially printed across the different brain regions following the “multi-trace systems consolidation” mechanism.…”

Switches to slow rhythmic neuronal activity lead to a plasticity-induced reset in synaptic weights

“…On the other hand, the homeostatic reset disrupts any learning that occurred during the previous period, which could lead to catastrophic forgetting (González et al, 2020). This forgetting may be overcome via mechanisms that transfer learning encoded in synaptic weight into long-lasting, structural changes in synaptic connections, such as the number of receptors at each synapse, the number and size of synapses, etc (Zenke and Gerstner, 2017; Luboeinski and Tetzlaff, 2021). Another possibility would be to exploit the homeostatic reset itself through neuromodulator-induced changes in synaptic rules (Pedrosa and Clopath, 2017; González-Rueda et al, 2018; Foncelle et al, 2018; Brzosko et al, 2017).…”