As shown in Fig. 9, NH125 treatment reduced the phosphorylation levels of eEF2 (Fig. 9a, c) and mTOR (Fig. 9a, b), while enhanced BDNF and eventually SNAP25 and PSD95 expression (Fig. 9a, d–f), suggesting an etiological role of eEF2 in LPS-induced synaptogenetic dysfunction and depression. This evidence concerns the gene SNAP25 and depressive disorder.