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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Psychol. | doi: 10.3389/fpsyg.2019.02394

Traumatic stress produces delayed alterations of synaptic plasticity in basolateral amygdala

Huan-Huan Zhang1, 2, Xin-Yi Guo1, 2, Jing-Liang Zhang3, 4,  Wen Zhang5,  Ya-Yun Chen5, Shi-Qiu Meng5,  Lin Lu5, 6, 7, Jian-Li Yang1, 2* and  Yan-Xue Xue5*
  • 1Tianjin Medical University, China
  • 2Tianjin Medical University General Hospital, China
  • 3State Key Laboratory of Natural and Biomimetic Drugs, Peking University, China
  • 4Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, United States
  • 5National Institute on Drug Dependence, Peking University, China
  • 6Peking University Sixth Hospital, China
  • 7Institute of Mental Health, Peking University, China

Exposure to acute traumatic stress events is a direct cause of post-traumatic stress disorder (PTSD). Amygdala is suggested to be involved in the development of PTSD. In our previous study, different activation patterns of glutamatergic and GABAergic neurons in early and late stages after stress were found. However, the neural plastic mechanism underlying the role of basolateral amygdala (BLA) in post-traumatic stress disorder remains unclear. Therefore, the main purpose of this study was to investigate time-dependent morphologic and electrophysiological changes in BLA during the development of PTSD. We established the rat model of PTSD using single prolonged stress (SPS) procedure. We found that 1 day after SPS, the rats showed normal anxiety behavior and there were no changes in either dendritic spine density or synaptic transmission in BLA. However, ten days after SPS, rats showed enhanced anxiety behavior in rats and increased density of spines in the BLA. The frequency of miniature excitatory and inhibitory postsynaptic currents in the BLA also increased 10 days after SPS exposure. Our results suggested that after traumatic stress, BLA displayed delayed increase in both spinogenesis and synaptic transmission, which may contribute to the development of PTSD.

Keywords: posttraumatic stress disorder, Single prolonged stress, basolateral amygdala, Dendritic Spines, synaptic plasiticty

Received: 20 Mar 2019; Accepted: 07 Oct 2019.

Copyright: © 2019 Zhang, Guo, Zhang, Zhang, Chen, Meng, Lu, Yang and Xue. 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. Jian-Li Yang, Tianjin Medical University General Hospital, Tianjin, China, adyy005@163.com
Mx. Yan-Xue Xue, National Institute on Drug Dependence, Peking University, Beijing, 100871, Beijing Municipality, China, yanxuexue@bjmu.edu.cn