• Yong Lu, Junli Zhang, Lin Zhang, Shaokang Dang, Qian Su, Huiping Zhang, Tianwei Lin, Xiaoxiao Zhang, Yurong Zhang, Hongli Sun, Zhongliang Zhu, and Hui Li.
• Department of Neonatology, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 West Yanta Road, Yanta District, Xi'an, 710061, Shanxi, China.
• Neurochem. Res. 2017 Dec 1; 42 (12): 3456-3464.

AbstractThis study is to determine the role and mechanism of hippocampal acetylation in prenatal stress (PS) induced depression-like behavior of male offspring rats. PS-induced depression rat model was established. Sucrose preference and forced swim test were used to observe the behavior changes of male offspring rats. Hippocampal acetylation was induced by Trichostatin A injection. Quantitative real-time PCR and Western blot were used to determine the changes of AMPARs in acetylated hippocampus. The behavioral tests proved that AMPA was involved in the PS-induced depression-like behavior in offspring rats. Hippocampal acetylation significantly increased the preference to sucrose of PS-induced offspring rats and reduced the immobile time in forced swimming test, suggesting that acetylation could improve PS-induced depression-like behaviors. In addition, PS inhibited the expression levels of GluA1-3 subunits of AMPARs in the offspring hippocampus, while Hippocampal acetylation could reverse this effect by increasing GluA1-3 expression. PS-induced reduction of GluA1-3 subunits of AMPARs may be an important potential mechanism of offspring depression. Hippocampal acetylation may improve PS-induced offspring depression-like behavior through the enhanced expression of AMPARs (GluA1-3 subunits).

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