ePoster

DIFFERENT POPULATION ACTIVITY DYNAMICS DURING RECALL OF SPATIAL REPRESENTATIONS ACROSS DORSAL HIPPOCAMPAL CA1 AND CA3

Amritesh Sureshand 3 co-authors

Charles University

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-529

Presentation

Date TBA

Board: PS04-08PM-529

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DIFFERENT POPULATION ACTIVITY DYNAMICS DURING RECALL OF SPATIAL REPRESENTATIONS ACROSS DORSAL HIPPOCAMPAL CA1 AND CA3 poster preview

Event Information

Poster Board

PS04-08PM-529

Abstract

A sudden exchange of sensory inputs, each of them characterizing a unique environment, leads to quick, step-like shift between the corresponding CA3 hippocampal spatial representations, often followed by period of flickering between the two maps orchestrated by local theta oscillation, a consequence of competitive stimulus network processing. Previously we found that the newly activated map is transiently overexpressed in contrast to the deactivated one, as an increased number of cells gets coactivated, possibly to support the dominance of the representation that corresponds to the newly set sensory conditions (Zitricky and Jezek, 2019). The overexpressed spatial code yields an increased position coding error, mainly due to the fact that the excessively activated cells code more distant locations within the same hippocampal map. Is the retrieval-dependent overexpression of the spatial memory code specific to hippocampal CA3 or is it present in CA1 as well? A theoretical approach predicts that the increased excitation in CA3 should elicit a similar overexpression in the corresponding CA1 representation.
Here we present data recorded in dorsal hippocampal CA1 and CA3. We tested rats in the two environment-teleportation paradigm introduced by Jezek et al. (2011), which allows repetitive sudden transitions between the environments. In contrast to data obtained in CA3, we did not detect the overexpression phenomenon in hippocampal CA1. The interpretation is unclear so far. It can be caused by the absent collateral feedback architecture in CA1 and/or by feed-forward inhibitory inputs preventing CA1 from oversaturation. Supported by GACR-26-23770S and SVV-263774.

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