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Authors & Affiliations
Mate Sumegi, Gaspar Olah, Istvan Lukacs, Judit Heredi, Martin Blazsek, Judit Makara, Zoltan Nusser
Abstract
The rodent hippocampus is essential for spatial memory formation and navigation. Cognitive maps of each environment are created by a population of hippocampal pyramidal cells (PCs), some of which display spatially tuned firing (place cells). When an animal enters a novel environment, new spatially tuned firing (place fields: PFs) of PCs emerges. Place field formation in CA1 PCs has been proposed to rely on a well-established cellular mechanism called behavioural timescale synaptic plasticity (BTSP). During BTSP, a single occurrence of a long postsynaptic dendritic plateau potential and resulting somatic complex spike burst firing results in potentiation of presynaptic input synapses active within a few-seconds-long, asymmetric time window around the plateau. While BTSP is well established in CA1 PCs, whether it is the only mechanism inducing PF formation is unknown. Here we aimed to explore alternative mechanisms of PF formation using in vivo two-photon [Ca2+] imaging in Thy1-GCaMP6s mice. While head-restrained mice navigated in a familiar linear virtual track, many new PFs emerged spontaneously in PCs. Approximately half of the new PFs were formed with characteristic signatures of BTSP. However, we also identified PF formations with non-BTSP-like spatial and amplitude modulation. Intriguingly, in 25% of PCs showing BTSP-driven PF formation, we also observed large [Ca2+] transients (exceeding the amplitude of the BTSP-driven PF formation event) that failed to trigger new PFs. These findings suggest that BTSP does not solely govern PF formation, and that large amplitude somatic calcium events per se are neither necessary nor sufficient for initiating new PFs.