High-altitude hypoxia induces disorders of the brain-endocrine-immune network through activation of corticotropin-releasing factor and its type-1 receptors.
- Author:
Xue-Qun CHEN
1
;
Fan-Ping KONG
;
Yang ZHAO
;
Ji-Zeng DU
Author Information
1. Division of Neurobiology and Physiology, Department of Basic Medical Sciences, School of Medicine, Zhejiang University, Hangzhou 310058, China.
- Publication Type:Journal Article
- MeSH:
Altitude;
Animals;
Brain;
physiopathology;
Corticotropin-Releasing Hormone;
metabolism;
Hypothalamo-Hypophyseal System;
physiopathology;
Hypoxia;
physiopathology;
Pituitary-Adrenal System;
physiopathology;
Receptors, Corticotropin-Releasing Hormone;
metabolism;
Tibet
- From:
Chinese Journal of Applied Physiology
2012;28(6):481-487
- CountryChina
- Language:English
-
Abstract:
High-altitude hypoxia can induce physiological dysfunction and mountain sickness, but the underlying mechanism is not fully understood. Corticotrophin-releasing factor (CRF) and CRF type-i receptors (CRFR1) are members of the CRF family and the essential controllers of the physiological activity of the hypothalamo-pituitary-adrenal (HPA) axis and modulators of endocrine and behavioral activity in response to various stressors. We have previously found that high-altitude hypoxia induces disorders of the brain-endocrine-immune network through activation of CRF and CRFR1 in the brain and periphery that include activation of the HPA axis in a time- and dose-dependent manner, impaired or improved learning and memory, and anxiety-like behavioral change. Meanwhile, hypoxia induces dysfunctions of the hypothalamo-pituitary-endocrine and immune systems, including suppression of growth and development, as well as inhibition of reproductive, metabolic and immune functions. In contrast, the small mammals that live on the Qinghai-Tibet Plateau alpine meadow display low responsiveness to extreme high-altitude-hypoxia challenge, suggesting well-acclimatized genes and a physiological strategy that developed during evolution through interactions between the genes and environment. All the findings provide evidence for understanding the neuroendocrine mechanisms of hypoxia-induced physiological dysfunction. This review extends these findings.
