Moreover, the inhibition of GSK3β activity is necessary for rapid antidepressant effect of ketamine, which suggested that GSK3β activity plays an important role in antidepressant.57, 59 To date, although the effects of reducing hippocampal neurogenesis on producing depressive behaviors are controversial, it is confirmed that AHN is essential for the therapeutic effects of fluoxetine in stressed mice.60, 61, 62 Therefore, the rescue of CRS-induced depression-like behaviors by overexpressing Wnt2 or Wnt3 might be mediated by regulating the GSK3β activity and/or hippocampal neurogenesis. This evidence concerns the gene GSK3B and depressive symptom measurement.