High-altitude hypoxia induces disorders of the brain-endocrine-immune network through activation of corticotropin-releasing factor and its type-1 receptors / 中国应用生理学杂志
Chinese Journal of Applied Physiology
;
(6): 481-487, 2012.
Article
Dans Anglais
| WPRIM
| ID: wpr-358708
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.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Axe hypophyso-surrénalien
/
Encéphale
/
Corticolibérine
/
Récepteur CRH
/
Tibet
/
Altitude
/
Axe hypothalamohypophysaire
/
Hypoxie
/
Métabolisme
Limites du sujet:
Animaux
Pays comme sujet:
Asie
langue:
Anglais
Texte intégral:
Chinese Journal of Applied Physiology
Année:
2012
Type:
Article
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