Fig. 3.

Acute intraperitoneal administration of 7-CTKA rapidly increased p-GSK3β level, reversed the deficits in the mammalian target of rapamycin (mTOR) function and blocked the loss of postsynaptic protein caused by chronic mild stress (CMS). (A) Experimental procedure. Chronic mild stress decreased p-GSK3β level in the medial prefrontal cortex (mPFC) and had no effects on t-GSK3β. Systemic 7-CTKA administration rapidly increased the expression of p-GSK3β. The percentages of (B) p-GSK3β and (C) t-GSK3β in the mPFC are shown. Chronic mild stress decreased p-GSK3β protein levels in the hippocampus and did not change t-GSK3β. Systemic 7-CTKA treatment had no effects on the expression of p-GSK3β. The percentages of (D) p-GSK3β and (E) t-GSK3β in the hippocampus are shown. Representative Western blot images are shown on the bottom. (F) The levels of PSD95, p-p70s6k and p-rps6 in the mPFC were decreased by CMS, whereas acute 7-CTKA or ketamine administration increased the expression of these proteins. (G) The levels of PSD95, p70s6k and rps6 in the hippocampus were not altered by CMS, 7-CTKA or ketamine. The data are expressed as mean and standard error of the mean (n = 6). *p < 0.05, †p < 0.01, ‡p < 0.001, compared with corresponding control group. GSK3β = glycogen synthase kinase-3β; p = phosphorylated; p70s6k = p70s6 kinase; PSD95 = postsynaptic density protein 95; rps6 = ribosomal protein s6; t = total.