Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-61499
PROVIDER: PRJNA261321 | ENA |
REPOSITORIES: ENA
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Project description:Recombinant insect baculoviral vectors (BV) efficiently transduce several types of cells in the brain and can possibly be used for gene therapy for brain disorders. To verify the suitability of using these viral vectors to develop gene therapy strategies in the brain, and to evaluate our method of virus purification, we evaluated immune reactions upon acute administration of BV that were purified by ion-exchange membrane chromatography with high-speed centrifugation or high-speed centrifugation alone into the mouse brain using microarray global gene expression profiling. Adult male mice (Mus musculus) were administered with baculoviral vectors purified by membrane chromatography with high-speed centrifugation (MC+HS) or baculoviral vectors purified by high-speed centrifugation (HS) alone into the brain. We sought to compare the gene expression changes in the brain triggered by MC+HS-purified and HS-purified baculoviral vectors.
2015-11-21 | E-GEOD-75265 | biostudies-arrayexpress
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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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