Analysis of gene expression after chronic restraint stress in the animal model of depression

2003 Fiscal Year Final Research Report Summary

• Project/Area Number: 14570926
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Psychiatric science
• Research Institution: Yamaguchi University
• Principal Investigator: WATANABE Yoshifumi Yamaguchi University, School of Medicine, Professor, 医学部, 教授 (90182964)
• Co-Investigator(Kenkyū-buntansha): AOKI Takeya Yamaguchi University, University Hospital, Member of the medical staff, 医学部附属病院, 医員(臨床) ; TUCHIYA Ken Yamaguchi University, University Hospital, Research Associate, 医学部附属病院, 助手 (00346561) ; HASHIMOTO Manabu Yamaguchi University, University Hospital, Research Associate, 医学部附属病院, 助手 (80314805)
• Project Period (FY): 2002 – 2003
• Keywords: stress / vulnerability / Fisher 344 / hypothalamus / gene expression

Research Abstract

Stress is known to be involved in the development of psychopathologies such as depression. In the present study, we searched for differentially expressed genes in the two species of rats (Fisher 344 and Sprague-Dawley(SD)) after chronic restraint stress. Experiments were conducted by comparing gene expressions in three discrete brain areas (hypothalamus, hippocampus, and cerebral cortex) of male Fisher 344 rats, a valid stress-vulnerable model in comparison with those in male SD rats. We used the microarray system for screening differentially expressed genes in hypothalamus of the animals. Using PCR to confirm the mRNA amounts, we identified two genes whose expression levels differed between Fisher 344 and SD rats. In hypothalamus, transcript levels of cytochrome c oxidase (COX)(subunit IV) of Fisher 344 rats were lower than those of SD. In contrast, the levels of COX were higher in hippocampus of Fisher 344 rats than those of SD rats. The expressions of phosphorylase b kings e in the three brain areas of Fisher 344 rats were higher than those of SD rats. The alterations in expression of these two genes, which are related to processes of energy metabolism, may cause impairment of neuronal function after chronic stress and be related to the development of stress associated psychopathological disorders