Meanwhile, we found that exons I, II, IV, and VI were obviously decreased by CUS, which has been widely reported to act as functional exons implicated in psychiatric disorders [47], whereas CPT reversed the decreases in BDNF transcription by enhancing the expression of exons I, IV, and VI, which indicates that the complex regulation mechanisms of CUS-induced pathogenesis and CPT were involved in therapeutic activity of depression, which may be a consequence of their distinct subcellular localization, spatially restricted effects, or the regulation of different signaling pathways [48]. This evidence concerns the gene BDNF and depressive disorder.