Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA179129 | ENA |
REPOSITORIES: ENA
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Project description:Engrams are considered to be substrates for memory storage, and the functional dysregulation of the engrams leads to cognition impairment.However, the cellular basis for these maladaptive changes lead to the forgetting of memories remains unclear. Here we found that the expression of autophagy protein 7 (Atg7) mRNA was dramatically upregulated in aged DG engrams, and led to the forgetting of contextual fear memory and the activation of surrounding microglia.To determine mechanism by which autophagy in DG engrams activates the surrounding microglia, mice were co-injected AAV-RAM-Cre either with AAV-Dio-Atg7-Flag or AAV-Dio- EYFP in dorsal dentate gyrus to overexpress ATG7 in the DG memory engrams. Microglia were separated using magnetic-activated cell sorting and subjected to RNA-Seq in dorsal hippocampus .Bioinformatics analysis shown overexpression of Atg7 in dorsal DG memory engrams caused an increase in the expression of Tlr2 in the surrounding microglia.Depletion of Toll-like receptor 2/4 (TLR2/4) in DG microglia prohibited excessive microglial activation and synapse elimination induced by the overexpression of ATG7 in DG engrams, and thus prevented forgetting. Furthermore, the expression of Rac1, a Rho-GTPases which regulates active forgetting in both fly and mice, was upregulated in aged engrams. Optogentic activation of Rac1 in DG engrams promoted the autophagy of the engrams, the activation of microglia, and the forgetting of fear memory. Invention of the Atg7 expression and microglia activation attenuated forgetting induced by activation of Rac1 in DG engrams. Together, our findings revealed autophagy-dependent synapse elimination of DG engrams by microglia as a novel forgetting mechanism.
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Project description:The gene expression changes associated with memory acquisition, consolidation and reconsolidation–all active epochs in memory formation–have been well characterized in the rodent hippocampus. Less is known, however, of the changes in gene expression during the offline maintenance of memory. In this study, we measured the gene expression changes in the dorsal hippocampus of four mice three days after consolidation of an active place avoidance memory. We examined gene expression changes in a putative subset of memory-associated neurons by leveraging the immediate early gene in vivo tagging system of the Arc-Cre/flox- eYFP transgenic mouse line. Through spatial transcriptomics we found that memory trained animals exhibited spatially regionalized expression of genes involved in post-synaptic function in CA1, synaptic vesicle transport in CA3, and neuronal differentiation in DG. Surprisingly, these gene expression enrichments were not observed in eYFP mRNA positive spatial spots. To gain granularity into this finding, we carried out single nuclear RNA sequencing, which confirmed enrichment of differentially expressed genes associated with synaptic plasticity and post-synaptic signaling unique to each subregion in trained animals, but not from their eYFP mRNA positive nuclei. Notably, nuclei of hippocampal neurons were largely characterized by their down regulation of genes involved in ATP synthesis and cytoplasmic translation. Our results suggest that two overarching transcriptomic patterns contribute to the functional changes in hippocampal cells during offline memory maintenance: regionally distributed expression of genes linked to synaptic functions (with concomitant sparseness of memory-associated neuronal ensembles) and a reduction of metabolic activity related genes across hippocampal sub-regions.
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