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Early Life Stress and Depression

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Front. Psychiatry | doi: 10.3389/fpsyt.2018.00588

Inhibition of GALR1 in PFC alleviates depressive-like behaviors in postpartum depression rat model by upregulating CREB-BNDF and 5-HT levels

 Hui Li1, Tong Wang1, Cuige Shi2, Yutao Yang1, Xiaoxiao Li1 and  Zhiqing D. Xu1*
  • 1Capital Medical University, China
  • 2Department of Cell Biology, National Research Institute of Family Planning, China

Estrogen (E2) withdrawal is a core pathology mechanism for postpartum depression (PPD). Galanin (GAL), an estrogen-inducible neuropeptide has also been reported to be associated with depression. However, it still remains unclear which GAL receptors (GALRs) are involved in PPD pathologic process. In the present study, we discovered that the expression of GALR1, rather than GALR2/3, was upregulated with a region-specific pattern in the prefrontal cortex (PFC) of E2 withdrawal induced PPD model rats. Meanwhile, c-fos was also upregulated only in PFC in the same animal model. Injection of GALR1-siRNA into the bilateral PFC ameliorated depressive-like behavior of PPD rats, suggesting that the upregulation of GALR1 in PFC is involved in PPD. Moreover, Western Blot and HPLC assays demonstrated that the downregulation of CREB-BDNF signaling and 5-HT levels in the PFC of PPD rats were reversed after GALR1-siRNA injection. These comprehensive results suggest that the knock down of GALR1 in PFC alleviates depressive-like behaviors and reverse downregulation of CREB-BDNF and 5-HT levels in PPD rat model.

Keywords: Postpartum depression (PPD), Prefronal cortex, Galanin receptor 1, BDNF, CREB

Received: 16 Jul 2018; Accepted: 25 Oct 2018.

Edited by:

Fushun Wang, Nanjing University of Chinese Medicine, China

Reviewed by:

Marc Landry, Université de Bordeaux, France
Fang Liu, Centre for Addiction and Mental Health (CAMH), Canada
Long-Chuan Yu, Peking University, China  

Copyright: © 2018 Li, Wang, Shi, Yang, Li and Xu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Zhiqing D. Xu, Capital Medical University, Beijing, China,