ABSTRACT: Most significantly affected GOs by TST stress include Cellular localization, transport and migration such as Cellular macromolecule localization (GO:0070727), Intracellular transport (GO:0046907) and Intracellular protein transport (GO:0006886), metabolic processes such as Small molecule metabolic process (GO:0044281), Cellular amide metabolic process (GO:0043603) and Lipid metabolic process (GO:0006629), neuronal cell population differentiation and proliferation such as Neurogenesis (GO:0022008), Neuron differentiation (GO:0030182), Glial cell differentiation (GO:0010001), Central nervous system development (GO:0007417), Astrocyte differentiation (GO:0048708) and Gliogenesis (GO:0042063), and cell signaling such as G-protein-coupled receptor signaling pathway (GO:0007186), Negative regulation of signaling (GO:0023057), Positive regulation of signaling (GO:0023056), Response to endogenous stimulus (GO:0009719) and Regulation of intracellular signal transduction (GO:1902531). Peptide metabolic process (GO:0006518), Peptidyl amino acid modification (GO:0018193), Regulation of steroid biosynthetic process (GO:0050810) were also significantly enriched in the TST stress-induced mice brain. Top significantly enriched Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways by the stress response related DEGs between high-dose RE vs TST include mitogen-activated protein kinase (MAPK) signaling pathway, Chemokine signaling pathway, Neurotrophin signaling pathway, Cytokine-cytokine receptor interaction, GnRH signaling pathway, ErbB signaling pathway, Toll-like receptor signaling pathway, T cell receptor signaling pathway, B cell receptor signaling pathway, vascular endothelial growth factor (VEGF) signaling pathway, Long-term depression, NOD-like receptor signaling pathway, Insulin signaling pathway, Jak-STAT signaling pathway, Apoptosis, and mTOR signaling pathway.