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. Author manuscript; available in PMC: 2018 May 8.
Published in final edited form as: Neuropharmacology. 2016 Mar 9;107:111–121. doi: 10.1016/j.neuropharm.2016.03.012

Fig. 5. Molecular effects of SAHA in the HIP and PFC of Crtc1‒/‒ mice and WT littermates.

Fig. 5

(A) SAHA had no effect on Crtc1 expression in the HIP and PFC of WT mice (n=8 for both group). (B) Untreated Crtc1‒/‒ mice (n=8) displayed higher hippocampal Bdnf expression compared to WT mice (+p<0.05, vs. WT mice). SAHA had no effect on Bdnf expression of WT and Crtc1‒/‒ mice (n=8 for each group). In the PFC, SAHA significantly increased Bdnf levels of Crtc1‒/‒ mice (##p<0.01 vs. Crtc1‒/‒ Vehicle). (C) Hippocampal BdnfIV expression was unchanged among the different groups. In the PFC, vehicle-treated Crtc1‒/‒ mice showed a decreased expression of BdnfIV (+p<0.05, vs. WT Vehicle). SAHA treatment significantly restored BdnfIV expression in Crtc1‒/‒ mice (##p<0.01, vs. Crtc1‒/‒ mice Vehicle). (D-F) Effects of SAHA on the expression of Nr4a1-3. (D) Crtc1‒/‒ mice displayed lower levels of Nr4a1 expression than WT mice in the PFC (++p<0.01, vs. WT Vehicle). Desipramine increased Nr4a1 levels of WT mice in the HIP but had no effect in the PFC (**p<0.01, vs. WT Vehicle). (E) Nr4a2 expression was found to be lower in the PFC of Crtc1‒/‒ mice compared to WT mice (++p<0.01, vs. WT Vehicle). SAHA had no effect on Nr4a2 expression in Crtc1‒/‒ mice but increased its expression in the HIP and PFC of WT mice (*p<0.05, vs. WT Vehicle). (F) SAHA had no effect on Nr4a3 expression in the HIP of all groups. In the PFC, SAHA increased Nr4a3 expression of WT animal but had no effect on Crtc1‒/‒ mice (*p<0.05, vs. WT Vehicle). Data are mean ±SEM.