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Hippocampal neuronal nitric oxide synthase contributes to chronic stress-induced hypothalamic-pituitary-adrenal axis hyperactivity
ZHOU Qigang 1,ZHU Lijuan 2,CHEN Chen 2,LIU Mengying 2,SUN Weixiang 2,ZHU Dongya 2 *
1.Pharmacy School, Nanjing Medcial University
2.Pharmacy School, Nanjing Medcial University, Nanjing 210029
*Correspondence author
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Funding: Specialized Research Fund for the Doctoral Program of Higher Education （No.200803120008）
Opened online: 2 June 2011
Accepted by: none
Citation: ZHOU Qigang,ZHU Lijuan,CHEN Chen.Hippocampal neuronal nitric oxide synthase contributes to chronic stress-induced hypothalamic-pituitary-adrenal axis hyperactivity[OL]. [ 2 June 2011] http://en.paper.edu.cn/en_releasepaper/content/4429267
 
 
Hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis is a hallmark of major depression. Impairment of hippocampal glucocorticoid receptor (GR), a molecular believed to mediate the negative feedback of hippocampus on HPA axis, has been thought causally related to the hyperactivity of HPA axis in depression. However, the mechanisms for the impairment of hippocampal GR remain unknown. Here, we report that neuronal nitric oxide synthase (nNOS) acts as an important negative regulator of GR in adult hippocampus. More importantly, hippocampal nNOS mediates GR downregulation of stress-induced glucocorticoids, resulting in overexpression of hypothalamic corticotrophin-releasing factor (CRF), a peptide that governs HPA axis, and in glucocorticoids secretion, indicating hyperactivity of HPA axis.
Keywords:Depression; nNOS; HPA axis
 
 
 

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