Department of Biology, University of Ottawa, Ottawa, ON, Canada.
Department of Biological Sciences, University of Calgary, Calgary, AB, Canada.
Gen Comp Endocrinol. 2023 Sep 15;341:114332. doi: 10.1016/j.ygcen.2023.114332. Epub 2023 Jun 8.
The formation of dominance hierarchies in pairs of juvenile rainbow trout (Oncorhynchus mykiss) results in subordinate individuals exhibiting chronically elevated plasma cortisol concentrations. Cortisol levels reflect a balance between cortisol production, which is coordinated by the hypothalamic-pituitary-interrenal (HPI) axis in teleost fish, and negative feedback regulation and hormone clearance, which act to lower cortisol levels. However, the mechanisms contributing to the longer-term elevation of cortisol levels during chronic stress are not well established in fishes. The current study aimed to determine how subordinate fish maintain elevated cortisol levels, by testing the prediction that negative feedback and clearance mechanisms are impaired by chronic social stress. Plasma cortisol clearance was unchanged by social stress based on a cortisol challenge trial, hepatic abundance of the cortisol-inactivating enzyme 11-beta hydroxysteroid dehydrogenase type 2 (11βHSD2), and tissue fate of labelled cortisol. The capacity for negative feedback regulation in terms of transcript and protein abundances of corticosteroid receptors in the preoptic area (POA) and pituitary appeared stable. However, changes in 11βHSD2 and mineralocorticoid receptor (MR) expression suggest subtle regulatory changes in the pituitary that may alter negative feedback. The chronic cortisol elevation observed during social subordination likely is driven by HPI axis activation and compounded by dysregulated negative feedback.
在成对的幼年虹鳟（Oncorhynchus mykiss）中，支配等级的形成导致从属个体表现出慢性升高的血浆皮质醇浓度。皮质醇水平反映了皮质醇产生的平衡，在硬骨鱼中，皮质醇产生由下丘脑-垂体-肾上腺（HPI）轴协调，而负反馈调节和激素清除则作用于降低皮质醇水平。然而，在鱼类中，慢性应激期间皮质醇水平长期升高的机制尚未得到很好的确定。本研究旨在通过测试负反馈和清除机制因慢性社会应激而受损的预测来确定从属鱼类如何维持升高的皮质醇水平。基于皮质醇挑战试验，社会应激并未改变血浆皮质醇清除率、肝脏中皮质醇失活酶 11-β 羟类固醇脱氢酶 2（11βHSD2）的丰度以及标记皮质醇的组织命运。在视前区（POA）和垂体中糖皮质激素受体的转录和蛋白丰度方面，负反馈调节的能力似乎稳定。然而，11βHSD2 和盐皮质激素受体（MR）表达的变化表明垂体中的细微调节变化可能改变负反馈。在社会从属期间观察到的慢性皮质醇升高可能是由 HPI 轴激活驱动的，并因失调的负反馈而加剧。
