Biology subjects

Atucha, E.

Publications and source records attributed to Atucha, E..

4 recordsLinked to original sources

bioRxiv2026

Circuit-specific reorganization of hippocampal-entorhinal-prefrontal subnetworks supports memory recall across the lifespan

How memories reorganize across brain circuits as they age remains a central question in systems neuroscience. Systems consolidation is thought to progressively shift memory reliance from the hippocampus to distributed cortical networks, yet the contribution of cortical regions beyond the prefrontal cortex and the nature of this shift remains unclear. Here we define the circuit-level organization of remote memory recall across entorhinal, prefrontal, and hippocampal subregions. Using high-resolution activity mapping combined with causal manipulations that leverage natural memory decay, we adapted a murine object-location paradigm to examine memory recall across the lifespan. We find that recall of early remote memories (1 month) selectively depends on a LEC-hippocampal (CA1/CA3) circuit, whereas recall of older memories (6-12 months) recruits a distinct and broader network involving both LEC and MEC together with ACC and CA1. These findings reveal a temporally ordered, circuit-specific reconfiguration of hippocampo-cortical networks and identify the EC as a dynamic hub in remote memory retrieval. Our results refine prevailing systems consolidation theories by showing that memory consolidation is a circuit-specific and temporally ordered process, rather than a passive gradual phenomenon, and position the EC as a central and dynamic component of remote memory retrieval alongside the PFC. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=123 SRC="FIGDIR/small/743925v1_ufig.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@11d2922org.highwire.dtl.DTLVardef@177b02borg.highwire.dtl.DTLVardef@cf0a11org.highwire.dtl.DTLVardef@9e0668_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2023

Phase-locking of hippocampal CA3 neurons to distal CA1 theta oscillations selectively predicts memory performance

How the coordination of neuronal spiking activity and brain rhythms between hippocampal subregions supports memory function remains elusive. We studied interregional coordination of CA3 neuronal spiking activity with CA1 theta oscillations by recording electrophysiological signals along the proximodistal axis of the hippocampus in rats performing a high memory demand recognition memory task adapted from humans. We found that CA3 population spiking activity occurs preferentially at the peak of distal CA1 theta oscillations only when animals recalled previously encountered stimuli. In addition, decoding analyses revealed that only population cell firing of proximal CA3 together with that of distal CA1 can predict memory performance in the present non-spatial task. Overall, our work demonstrates an important role of the synchronization of CA3 neuronal activity with CA1 theta oscillations for successful recognition memory.

neuroscience↗

bioRxiv2021

Remembering the gist of an event over a lifetime depends on the hippocampus

A well-accepted view in memory research is that retrieving the gist of a memory over time depends on the cortex, typically the prefrontal cortex, while retrieving its precision relies on the hippocampus. More recent advances indicate that the hippocampal subfield CA1, as opposed to CA3, remains engaged even for retrieving very remote memories and that this engagement coincides with a maximal recruitment of parahippocampal cortical areas (LEC, MEC, PER and POR)1. Using a time-window comparable to that used in human long-term memory studies, here we show that CA1 is necessary for retrieving the gist of a memory independently of its age while memory precision specifically depends on CA3 in a time-dependent manner. The precision for the memory of a context-footshock association was tested in mice after one day or very remotely (i.e. after 6 months or one year) allowing for the natural fading of the memory trace. Retrieving recent memories engaged both CA1 and CA3 in control mice as revealed by high levels of RNA of the immediate-early gene Arc, strongly tied to synaptic plasticity and memory function. Optogenetic inhibition of CA3 cell firing led to the loss of memory precision, i.e. the retrieval of the gist memory selectively supported by CA1. In contrast, CA1 inhibition abolished memory retrieval and reduced both CA1 and CA3s activity. At very remote tests, controls retrieved only the gist of the event by recruiting CA1 and parahippocampal areas. Retrieving this gist was selectively abrogated upon CA1 optogenetic inactivation that dramatically reduced parahippocampal activity. Our findings indicate that the hippocampus, specifically CA1, is required for gist memory retrieval even for very remote memories that were previously reported to be hippocampal-independent, while CA3 is necessary for recalling precise memories in a time-dependent manner.

neuroscience↗

bioRxiv2020

Recognition memory: familiarity signals increase selectively in the lateral entorhinal cortex following hippocampal lesions

The sense of familiarity for events is crucial for successful recognition memory. However, the neural substrate and mechanisms supporting familiarity remain unclear. Some human and animal studies suggest that the lateral entorhinal (LEC) and the perirhinal (PER) cortices might be essential for familiarity judgments while others attribute this function to the hippocampus (HIP) and it is unclear whether LEC, PER and HIP interact within this frame. Here, we especially investigate if LEC and PERs contribution to familiarity depends on hippocampal integrity. Using a human to rat translational memory task and high resolution IEG imaging, we report that hippocampal lesions selectively enhance activity in LEC during familiarity judgments. These findings suggest that different mechanisms support familiarity in LEC and PER and, that HIP might exert a tonic inhibition on LEC during recognition memory that might be released when HIP is compromised, possibly constituting a compensatory mechanism in aging and amnesic patients.

neuroscience↗