Stress-restress: Effects on ACTH and fast feedback

Stress-restress: Effects on ACTH and fast feedback
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DOI:
10.1016/s0306-4530(97)00044-9
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发表时间:
1997-08-01
影响因子:
3.7
通讯作者:
Young, EA
Young, EA
中科院分区:
医学2区
文献类型:
--
作者:
Liberzon, I;Krstov, M;Young, EA

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糖皮质激素的分泌受到负反馈的严格调节。糖皮质激素反馈已被发现改变抑郁症和创伤后应激障碍(PTSD)。虽然在抑郁症中发现了低敏感性糖皮质激素反馈,但在PTSD中描述了过度敏感或增强的负反馈。增强的负反馈可被看作是HPA轴抑制成分的致敏作用,应激-再应激或时间依赖性致敏(TDS)模型被认为是PTSD的动物模型。我们研究了该模型对HPA轴的影响,以确定它是否会增加对PTSD患者中发现的负反馈的敏感性。将成年Sprague-Dawley雄性大鼠暴露于单次长时间应激(束缚,随后强迫游泳并暴露于乙醚蒸汽),并在7天后短暂再应激。在两项研究中评估了单次长时间应激对血浆ACTH和皮质酮反应(0,5和30分钟)以及糖皮质激素快速反馈(皮质醇与生理盐水预处理)的影响。暴露于单次长时间I:tress的动物与未处理动物相比显示出增强的负反馈(F = 4.6371,df = 3,p = 0.0107),但在再应激期间ACTH或皮质酮反应没有差异。皮质醇预处理,在第一个压力会议,并没有阻止发展的增强快速反馈时,再强调。这可以被看作是HPA轴的抑制元件的敏化,提示应激-再应激范式可能作为PTSD患者中发现的HPA异常的良好动物模型。出版社:Elsevier Science Ltd
Glucocorticoid secretion is tightly regulated by negative feedback. Glucocorticoid feedback has been found to be altered in depression and post-traumatic stress disorder (PTSD). While hyposensitive glucocorticoid feedback has been found in depression, hypersensitive or enhanced negative feedback was described in PTSD. Enhanced negative feedback, can be seen as a sensitization of the inhibitory elements of HPA axis, and stress-restress or time dependent sensitization (TDS) model, has been suggested as an animal model for PTSD. We have studied the effects of this model on the HPA axis to determine whether it will produce increased sensitivity to negative feedback as found in PTSD patients. Adult Sprague-Dawley male rats were exposed to a single session of prolonged stress (restraint followed by a forced swim and exposure to ether vapors) and briefly restressed 7 days later. The effects of single prolonged stress on plasma ACTH and corticosterone responses (0, 5, and 30 min) and on glucocorticoid fast feedback (cortisol vs. saline pretreatment) were assessed in two studies. Animals exposed to single prolonged I:tress showed enhanced negative feedback in comparison to naive animals (F = 4.6371, df = 3, p = .0107), but there was no difference in ACTH or corticosterone responses during the restress. Pretreatment with cortisol, in the first stress session, did not prevent the development of the enhanced fast feedback when restressed. This can be seen as a sensitization of the inhibitory elements of HPA axis, suggesting that stress-restress paradigm might serve as a good animal model for HPA abnormalities found in PTSD patients. Published by Elsevier Science Ltd.