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Neural Plasticity
Volume 2018 (2018), Article ID 9360203, 11 pages
Research Article

Recovery of Chronic Stress-Triggered Changes of Hippocampal Glutamatergic Transmission

1Department of Psychology, Zhejiang Sci-Tech University, Hangzhou, Zhejiang, China
2Shanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China
3Co-innovation Center of Neuroregeneration, Nantong University, Nantong, Jiangsu, China

Correspondence should be addressed to Gonglin Hou and Ti-Fei Yuan

Received 3 August 2017; Revised 6 November 2017; Accepted 28 November 2017; Published 30 January 2018

Academic Editor: Fang Pan

Copyright © 2018 Min Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic stress results in neurochemical, physiological, immune, molecular, cellular, and structural changes in the brain and often dampens the cognition. The hippocampus has been one major focus in studying the stress responsivity and neural mechanisms underlying depression. Both acute and chronic stress stimuli lead to dynamic changes in excitatory transmission in the hippocampus. The present study examined the potential effects of spontaneous recovery after chronic stress on spatial memory function and glutamatergic transmission in the hippocampus. The results showed that chronic unpredicted mild stress transiently increased AMPA receptor GluA2/3 subunit expression, together with elevated PICK-1 protein expression. Spontaneous recovery restored the behavioral deficits in Barnes maze test, as well as the glutamate receptor expression changes. In conclusion, spontaneous recovery acts as an important mechanism in system homeostasis.