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. 2015 Mar 6;18(8):pyv010. doi: 10.1093/ijnp/pyv010

Figure 4.

Figure 4.

Tetramethylpyrazine (TMP) treatment reverses the chronic social defeat stress (CSDS)-induced decrease of the brain-derived neurotrophic factor (BDNF) signaling pathway. (A) Western blotting results showed that TMP treatment restored the CSDS-induced decrease of BDNF, phospho-extracellular regulated protein kinase 1/2 (pERK1/2), the active form of protein kinase B (pAKT), and phospho-cAMP response element binding protein (pCREB) protein levels in the hippocampus. CSDS + TMP mice displayed significantly higher hippocampal expression of BDNF, pERK1/2, pAKT and pCREB than CSDS + vehicle mice. (B) As in the hippocampus, TMP administration also restored the CSDS-induced inhibition of BDNF, pERK1/2, pAKT, and pCREB levels in the medial prefrontal cortex (mPFC). CSDS + TMP mice displayed higher BDNF, pERK1/2, pAKT, and pCREB expression in the mPFC, compared to CSDS + vehicle mice. Data are expressed as means ± standard error of the mean (n = 5); * p < 0.01 vs. vehicle control; # p < 0.05, ## p < 0.01 vs. CSDS + vehicle group. Comparison was made by two-way analysis of variance followed by a post hoc Bonferroni’s test. AKT, PI3K–protein kinase B; CREB, cyclic Adenosine monophosphate (cAMP) response element-binding protein; ERK, extracellular regulated protein kinase; glyceraldehyde-3-phosphate dehydrogenase (GAPDH).