RESUMO
Episodic memory is a recollection of past personal experiences associated with particular times and places. This kind of memory is commonly subject to loss of contextual information or" semantization", which gradually decouples the encoded memory items from their associated contexts while transforming them into semantic or gist-like representations. Novel extensions to the classical Remember/Know behavioral paradigm attribute the loss of episodicity to multiple exposures of an item in different contexts. Despite recent advancements explaining semantization at a behavioral level, the underlying neural mechanisms remain poorly understood. In this study, we suggest and evaluate a novel hypothesis proposing that Bayesian-Hebbian synaptic plasticity mechanisms might cause semantization of episodic memory. We implement a cortical spiking neural network model with a Bayesian-Hebbian learning rule called Bayesian Confidence Propagation Neural Network (BCPNN), which captures the semantization phenomenon and offers a mechanistic explanation for it. Encoding items across multiple contexts leads to item-context decoupling akin to semantization. We compare BCPNN plasticity with the more commonly used spike-timing dependent plasticity (STDP) learning rule in the same episodic memory task. Unlike BCPNN, STDP does not explain the decontextualization process. We further examine how selective plasticity modulation of isolated salient events may enhance preferential retention and resistance to semantization. Our model reproduces important features of episodicity on behavioral timescales under various biological constraints whilst also offering a novel neural and synaptic explanation for semantization, thereby casting new light on the interplay between episodic and semantic memory processes.Significance StatementRemembering single episodes is a fundamental attribute of cognition. Difficulties recollecting contextual information is a key sign of episodic memory loss or semantization. Behavioral studies demonstrate that semantization of episodic memory can occur rapidly, yet the neural mechanisms underlying this effect are insufficiently investigated. In line with recent behavioral findings, we show that multiple stimulus exposures in different contexts may advance item-context decoupling. We suggest a Bayesian-Hebbian synaptic plasticity hypothesis of memory semantization and further show that a transient modulation of plasticity during salient events may disrupt the decontextualization process by strengthening memory traces, and thus, enhancing preferential retention. The proposed cortical network-of-networks model thus bridges micro and mesoscale synaptic effects with network dynamics and behavior.
RESUMO
We present an electrophysiological model of double bouquet cells and integrate them into an established cortical columnar microcircuit model that has previously been used as a spiking attractor model for memory. Learning in that model relies on a Hebbian-Bayesian learning rule to condition recurrent connectivity between pyramidal cells. We here demonstrate that the inclusion of a biophysically plausible double bouquet cell model can solve earlier concerns about learning rules that simultaneously learn excitation and inhibition and might thus violate Dale's principle. We show that learning ability and resulting effective connectivity between functional columns of previous network models is preserved when pyramidal synapses onto double bouquet cells are plastic under the same Hebbian-Bayesian learning rule. The proposed architecture draws on experimental evidence on double bouquet cells and effectively solves the problem of duplexed learning of inhibition and excitation by replacing recurrent inhibition between pyramidal cells in functional columns of different stimulus selectivity with a plastic disynaptic pathway. We thus show that the resulting change to the microcircuit architecture improves the model's biological plausibility without otherwise impacting the model's spiking activity, basic operation, and learning abilities.
