期刊
BEHAVIOURAL BRAIN RESEARCH
卷 362, 期 -, 页码 288-298出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbr.2019.01.026
关键词
Depression; Anxiety; Cell proliferation; Serotonin; Glucocorticoids; Mineralocorticoid receptor
资金
- National Natural Science Foundation of China [81274122, 81202507, U1402221, 81573636]
- National Mega-project for Innovative Drugs [2012ZX09301002-004, 2012ZX09301002-001]
- Program for Changjiang Scholars and Innovative Research Team in University (PCSIRT) [IRT1007]
- Specialized Research Fund for the Doctoral Program of Higher Education of China [20121106130001]
- Beijing Natural Science Foundation [7131013, 7142115]
- Beijing Key Laboratory of New Drug Mechanisms and Pharmacological Evaluation Study [BZ0150]
- State Key Laboratory Fund Open Project [GTZK201610]
- China Postdoctoral Science Foundation [2013M540066]
Glucocorticoids are vital stress response hormones and facilitate stress coping. However, sustained glucocorticoid exposure is associated with negative effects on brain. The precise role of glucocorticoids in depression and anxiety remains unclear. In the present study, we found that rats exposed to chronic unpredictable stress (CUS) showed anxiety-like behavior but not depressive-like behavior in the absence of glucocorticoid production. It was interesting to find that the level of serotonin (5-HT) and the expression of tryptophan hydroxylase-2 (TPH2) were decreased after CUS in the hippocampus in sham rats, while adrenalectomy (ADX) prevented such decreases. In addition, the neurogenesis in hippocampus decreased in both sham and ADX rats after stress exposure. Furthermore, inhibition of mineralocorticoid receptor (MR) with spironolactone induced anxiety like behavior in sham rats but not ADX rats. The proliferation of cells was blocked by spironolactone. In conclusion, our results indicate that MR-dependent neurogenesis was closely related with anxiety-like behavior.
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