The astrocytic ensemble is a multiday eligibility trace stabilizing memory
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136834 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Recalled memories become transiently labile and require stabilization. The mechanism for specifically stabilizing memories of critical experiences essential for survival, which are often emotionally salient and repeated, remains unclear. Here, we identified an astrocytic ensemble that is transcriptionally primed by emotional experience and functionally triggered by repeated experience to stabilize labile memory. Using our novel brain-wide Fos tagging and imaging method, we found that astrocytic Fos ensembles were preferentially recruited in regions with neuronal engrams and were more widespread during fear recall than conditioning. We established the induction mechanism of the astrocytic ensemble, which involves two steps: (i) an initial fear experience inducing day-long, slow astrocytic state changes with noradrenaline (NA) receptor upregulation, and (ii) enhanced NA responses during recall, a repeated experience, enabling astrocytes to integrate coincident signals from local engrams and long-range NA projections, inducing secondary astrocytic state changes, including the upregulation of Fos and the neuromodulatory molecule Igfbp2. Pharmacological and genetic perturbation of the astrocytic ensemble signaling modulate engrams, and memory stability and precision. The astrocytic ensemble therefore is as a multiday trace left in a subset of astrocytes after experience-dependent neural activity, making them eligible to capture future repeated experiences for stabilizing memories.
2025-08-28 | GSE272414 | GEO
Project description: Not available
| S-EPMC12675280 | biostudies-literature
Project description:TRACE-RICE_Genomic_data_rice_variety_authentication
| PRJEB64146 | ENA
Project description:Associating temporally discontinuous events is one of the key characters of episodic memory. In trace fear conditioning (TFC), the CA1-subiculum (SUB) complex is required for tone-shock associations over a temporal trace, while the retrosplenial cortex (RSP) serves as a hub for temporal coding. How these regions interact during TFC remains unclear. Here, we show that molecularly distinct VGluT1 and VGluT2 SUB to RSP projections redundantly contribute to the associative component of TFC, whereas VGluT2 SUB to RSP projections selectively processes the temporal component. In these projections, trace memory formation was associated with increased and decreased bulk calcium activity at tone and trace onset, respectively, an activity pattern that was reestablished during memory recall. Such pattern was not observed in CA subfields, suggesting that associations and temporal gaps of TFC are integrated at the SUB before being presented to the RSP. Our findings establish a circuit mechanism for representing complex temporal information in episodic memory.
2025-05-30 | MSV000098056 | MassIVE
Project description:Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory
| PRJNA635818 | ENA
Project description:Gene expression profiling following different learning paradigms may help in defining the moleular pathways of memory formation. In this study we analyzed the gene expression pattern of murine hippocampus at different time points (0.5 h, 2h, 6h) after trace fear conditioning. We compared trained mice with naive mice that remained in their homecages. Keywords: Time course We used 3 arrays for each experimental condition. Each array was hybridized witha a pool of RNA of 6 animals.
2010-05-27 | E-GEOD-16158 | biostudies-arrayexpress
Project description:The excitatory amino acid transporter 2 (EAAT2) is the major glutamate transporter in the brain expressed predominantly in astrocytes and at low levels in neurons and axonal terminals. EAAT2 expression is reduced in aging and sporadic Alzheimer’s disease (AD) patients’ brains. The role EAAT2 plays in cognitive aging and its associated mechanisms remains largely unknown. Here, we show that conditional deletion of astrocytic and neuronal EAAT2 results in age-related cognitive deficits. Astrocytic, but not neuronal EAAT2, deletion leads to early deficits in short-term memory and in spatial reference learning and long-term memory. Neuronal EAAT2 loss results in late-onset spatial reference long-term memory deficit. Neuronal EAAT2 deletion leads to dysregulation of the kynurenine pathway, and astrocytic EAAT2 deficiency results in dysfunction of innate and adaptive immune pathways, which correlate with cognitive decline. Astrocytic EAAT2 deficiency also shows transcriptomic overlaps with human aging and AD. Overall, the present study shows that in addition to the widely recognized astrocytic EAAT2, neuronal EAAT2 plays a role in hippocampus-dependent memory. Furthermore, the gene expression profiles associated with astrocytic and neuronal EAAT2 deletion are substantially different, with the former associated with inflammation and synaptic function similar to changes observed in human AD and gene expression changes associated with inflammation similar to the aging human brain.
2021-03-18 | GSE169083 | GEO
Project description:Gene expression profiling following different learning paradigms may help in defining the moleular pathways of memory formation. In this study we analyzed the gene expression pattern of murine hippocampus at different time points (0.5 h, 2h, 6h) after trace fear conditioning. We compared trained mice with naive mice that remained in their homecages. Keywords: Time course
2010-05-06 | GSE16158 | GEO
Project description:Astrocytes support synaptic activity and associated circuit function, including those linked to sleep and memory, though how they coordinate these processes remains poorly defined. Here we show that the transcription factor Nuclear Factor I-X (NFIX) is required to maintain astrocyte function in the thalamic reticular nucleus (TRN), as its deletion results in aberrant thalamocortical oscillations and impaired memory formation. We found that NFIX directly regulates the expression of monoamine oxidase B (MAOB) and the purinergic receptor P2RX7. Mechanistically, knockdown of Maob or knockout of P2rx7 in TRN astrocytes results in decreased astrocytic release of the neurotransmitter GABA, reducing tonic inhibition of ventrobasal (VB) relay neurons and impairing memory formation. Altogether, our studies identify region-specific roles for astrocytic NFIX and its gene regulatory network in TRN astrocytes, while further revealing that astrocytes in the TRN couple regulation of thalamocortical circuit dynamics and memory formation through parallel GABA and purinergic signaling pathways.
2026-08-13 | GSE309186 | GEO
Project description:Astrocytic ApoE reprograms neuronal cholesterol metabolism and histone acetylation mediated memory [RNA-seq]
| PRJNA635821 | ENA