Dinan Timothy G, Scott Lucinda V
Department of Psychiatry and Alimentary Pharmabiotic Centre, Cork University Hospital, Ireland.
J Anat. 2005 Sep;207(3):259-64. doi: 10.1111/j.1469-7580.2005.00443.x.
Overactivity of the hypothalamic-pituitary-adrenal (HPA) axis characterized by hypercortisolism, adrenal hyperplasia and abnormalities in negative feedback is the most consistently described biological abnormality in melancholic depression. Corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) are the main secretagogues of the HPA/stress system. Produced in the parvicellular division of the hypothalamic paraventricular nucleus the release of these peptides is influenced by inputs from monoaminergic neurones. In depression, anterior pituitary CRH1 receptors are down-regulated and response to CRH infusion is blunted. By contrast, vasopressin V3 receptors on the anterior pituitary show enhanced response to AVP stimulation and this enhancement plays a key role in maintaining HPA overactivity.
以高皮质醇血症、肾上腺增生和负反馈异常为特征的下丘脑-垂体-肾上腺(HPA)轴功能亢进是忧郁症中最常被描述的生物学异常。促肾上腺皮质激素释放激素(CRH)和精氨酸加压素(AVP)是HPA/应激系统的主要促分泌素。这些肽在下丘脑室旁核小细胞部产生,其释放受单胺能神经元输入的影响。在抑郁症中,垂体前叶CRH1受体下调,对CRH输注的反应减弱。相比之下,垂体前叶的加压素V3受体对AVP刺激的反应增强,这种增强在维持HPA轴功能亢进中起关键作用。