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:Experience-dependent learning depends on synaptic plasticity. Recent findings show that effective integration of novel salient information requires coordinated processes of homo- and hetero- synaptic plasticity onto neighboring dendritic branches. In this work, we hypothesized that activity-dependent remodeling of the peri-synaptic extracellular matrix (ECM) contributes to this mechanism. We show that clusters of the peri-synaptic ECM proteoglycans, containing 6- and 2,6-sulfated chondroitin sulfates recognized by CS56 antibody, emerge in response to sensory stimuli, showing temporal and spatial coincidence with dendritic spine plasticity. CS56 co-immunoprecipitation of synaptosomal proteins identified several CS56-carrying/binding synaptic molecules that are implicated in Ca2+ signaling, vesicles cycling and AMPA-receptor exocytosis, thus suggesting their pivotal role in long-term potentiation (LTP). Finally, we demonstrated that the attenuation of CS56 glycoepitopes in the CA1 hippocampal region, through the depletion of versican as one of its main carriers, impairs LTP and object location memory in adult mice. These findings show that specific ECM glycans regulates the molecular mechanisms underlying induction and consolidation of synaptic plasticity, confirming that experience-dependent refinement of the brain ECM plays a critical role in learning and memory.
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