首页 | 本学科首页   官方微博 | 高级检索  
     


Increased Phosphorylation of Extracellular Signal-Regulated Kinase in the Medial Prefrontal Cortex of the Single-Prolonged Stress Rats
Authors:Hai-Tao Wang  Fang Han  Jun-Ling Gao  Yu-Xiu Shi
Affiliation:(1) Department of Histology and Embryology, Basic Medical Sciences College, China Medical University, 92 North 2nd Road, 110001 Shenyang, China;(2) Department of Histology and Embryology, North China Coal Medical University, No.57 Jianshe Road, 063000 Tangshan, China;
Abstract:The purpose of this study is to investigate the change of phosphorylated p44/42 extracellular signal-regulated kinase (pERK1/2) and c-fos expression induced by single-prolonged stress (SPS) in medial prefrontal cortex (mPFC), and to determine whether extracellular signal-regulated kinase (ERK) pathway plays a role in SPS. Before exposure to SPS, Wistar rats were bilaterally infused with PD98059, inhibitor of ERK, into the mPFC. Animals were then tested in the open field (OF), elevated plus-maze (EPM), and Morris water maze (MWM). Brains were removed for immunohistochemical staining and Western blotting of pERK1/2. And reverse transcription-polymerase chain reaction (RT-PCR) was employed to detect the c-fos mRNA, a member of immediate early genes (IGEs) family. SPS exposure resulted in pronounced anxiety-like behavior compared to control animals. SPS-exposed animals also displayed marked learning and spatial memory impairments. PD98059 significantly ameliorated anxiety-like behavior, learning, and spatial memory impairments. Expression of pERK1/2 in mPFC was significantly increased after rats were exposed to SPS, and the increase induced by SPS was significantly abolished by PD98059. The results of RT-PCR showed that the expression of c-fos mRNA had a significant increase in SPS rats compared with control rats, and the increase was significantly abolished by PD98059. The results suggest that pERK1/2 may be related to signal transduction pathway in single-prolonged stress.
Keywords:
本文献已被 SpringerLink 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号