Fig. 7: CaMKIIα in the PL is a critical player in regulating depressive behavior.

a Transcript levels of GABRα1 and GABRβ2 in the PL of the CON, CRST, RS5, and CORT (0.1 mg kg⁻¹) groups. Tissue sample groups were prepared from the experiments depicted in Fig. 4g, h (n = 7–12 per group). b–g Experimental design (b). Picrotoxin (PTX) was infused through a pre-implanted cannula into the PL of CRST and RS5-treated mice, and behavior tests were carried out 60–90 min after drug infusion on post-stress day 22 (b). Western blots showing the expression levels of p-CaMKIIα, CaMKIIα, p-ERK1/2, ERK1/2, and β-actin in the PL of the indicated groups (c). Quantification levels of p-CaMKIIα (d) and p-ERK1/2 (e). Western blots were representative of three technical repeats carried out using tissue samples from four pooled animals per group. β-actin was included as an internal loading control. Immobility time in the TST (f) and FST (g) for the indicated groups (n = 8 animals per group). h–k Experimental design (h). KN62 (2.5 nmol per injection) was infused into the PL through a pre-implanted cannula. After 60 min, behavioral tests were performed in the order SIT, TST, and FST. The % time of social interaction in the SIT (i) and immobility time in the TST (j) and FST (k) for the indicated groups (n = 7 animals per group). l–q Experimental design (l). Transcript levels showing siRNA-mediated knockdown of CaMKIIα (m) and ERK1 (n) in the PL, and behavioral tests were carried out 2 days later. The % time of social interaction in the SIT (o), and immobility time in the TST (p) and FST (q) for the indicated groups (n = 8 animals per group). Data were mean ± SEM. Gray circles represent individual data points. *, the difference compared to control; #, the difference compared to CRST. *, #, p < 0.05, **, ##, p < 0.01 (Two-sided Student’s t-test; one-way ANOVA followed by Newman–Keuls post hoc test). See Supplementary Data 4 for statistical details.