Dendritic Inhibition Effects in Memory Retrieval of a Neuromorphic Microcircuit Model of the Rat Hippocampus

TL;DR

This study explores how dendritic inhibition in the rat hippocampus helps ensure accurate memory retrieval by controlling which neurons fire during memory recall.

Contribution

The paper reveals distinct roles of apical dendritic inhibition in preventing interference and ensuring precise memory retrieval in a computational model.

Findings

Apical dendritic inhibition prevents non-engram cells from firing during memory retrieval, ensuring only engram cells are active.

Inhibition in the apical tuft reduces interference from spurious inputs during recall, especially when engram cell populations are large.

Removing apical tuft inhibition disrupts recall performance when non-engram cells are activated by external cues.

Abstract

Background: Studies have shown that input comparison in the hippocampus between the Schaffer collateral (SC) input in apical dendrites and the perforant path (PP) input in the apical tufts dramatically changes the activity of pyramidal cells (PCs). Equally, dendritic inhibition was shown to control PC activity by minimizing the depolarizing signals in their dendritic trees, controlling the synaptic integration time window, and ensuring temporal firing precision. Objectives: We computationally investigated the diverse roles of inhibitory synapses on the PC dendritic arbors of a CA1 microcircuit model in mnemonic retrieval during the co-occurrence of SC and PP inputs. Results: Our study showed inhibition in the apical PC dendrites mediated thresholding of firing during memory retrieval by restricting the depolarizing signals in the dendrites of non-engram cells, thus preventing them from firing, and ensuring perfect memory retrieval (only engram cells fire). On the other hand, inhibition in the apical dendritic tuft removed interference from spurious EC during recall. When EC drove only the engram cells of the SC input cue, recall was perfect under all conditions. Removal of apical tuft inhibition had no effect on recall quality. When EC drove 40% of engram cells and 60% of non-engram cells of the SC input cue, recall was disrupted, and this disruption was worse when the apical tuft inhibition was removed. When EC drove only the non-engram cells of the cue, then recall was perfect again but only when the population of engram cells was small. Removal of the apical tuft inhibition disrupted recall performance when the population of engram cells was large. Conclusions: Our study deciphers the diverse roles of dendritic inhibition in mnemonic processing in the CA1 microcircuit of the rat hippocampus.

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