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大鼠中脑水管周围灰质刺激引起逃避反应或惊恐发作后血浆皮质酮水平升高。

Increased plasma corticosterone levels after periaqueductal gray stimulation-induced escape reaction or panic attacks in rats.

机构信息

Department of Neuroscience, Maastricht University, The Netherlands.

出版信息

Behav Brain Res. 2011 Apr 15;218(2):301-7. doi: 10.1016/j.bbr.2010.12.026. Epub 2010 Dec 24.

Abstract

The hypothalamo-pituitary-adrenal (HPA) axis is involved in stress, depression and anxiety. Controversy exists on HPA axis activation during panic attacks (PAs). We examined whether the HPA axis is involved in the escape or panic-like response in an animal model of PAs induced by electrical stimulation of the dorsolateral periaqueductal gray (dlPAG) in rats. Additionally, rats were also treated with chronic administration of buspirone (BUSP) and escitalopram (ESCIT), respectively; and they were stimulated in the open-field arena for panic-like reaction. Levels of stress hormone corticosterone were measured following 30 min after escape or panic condition. Our results demonstrated that the levels of plasma corticosterone were significantly increased after the induction of escape or panic-like response in comparison with the sham animals. The levels of corticosterone were significantly decreased in the dlPAG stimulated groups after rats were treated chronically with the ESCIT but not the BUSP as compared to the saline treated animals. Importantly, the increase of corticosterone level after escape or panic-like response was paralleled by an increase of neuronal activation of c-Fos in both the parvocellular and magnocellular paraventricular nucleus of the hypothalamus. Moreover, the c-Fos data also showed a decrease in the number of positive cells particularly for the ESCIT as well as the BUSP in comparison with the saline stimulated animals. In conclusion, the present study clearly demonstrated that PA or escape response activates the HPA axis and it remains difficult to anticipate the mechanism underlying HPA axis during PAs and its relationship with 5-HT drugs.

摘要

下丘脑-垂体-肾上腺 (HPA) 轴参与应激、抑郁和焦虑。在惊恐发作 (PAs) 期间 HPA 轴的激活存在争议。我们研究了在电刺激大鼠背外侧缰状核 (dlPAG) 诱导的 PAs 动物模型中,HPA 轴是否参与逃避或类似惊恐反应。此外,大鼠还分别接受了慢性丁螺环酮 (BUSP) 和依地普仑 (ESCIT) 治疗;并在开阔场中刺激以产生类似惊恐反应。在逃避或惊恐条件 30 分钟后测量应激激素皮质酮的水平。

我们的结果表明,与假手术动物相比,在诱导逃避或类似惊恐反应后,血浆皮质酮水平显著升高。与生理盐水处理的动物相比,ESCIT 处理的大鼠在 dlPAG 刺激后,皮质酮水平显著降低,但 BUSP 处理的大鼠则不然。重要的是,在逃避或类似惊恐反应后皮质酮水平的增加与下丘脑室旁核中小细胞和大细胞 parvocellular 和 magnocellular 的神经元激活 c-Fos 的增加平行。此外,与生理盐水刺激的动物相比,c-Fos 数据还显示 ESCIT 和 BUSP 处理的动物阳性细胞数量减少。

总之,本研究清楚地表明,PA 或逃避反应激活了 HPA 轴,并且仍然难以预测 PAs 期间 HPA 轴的机制及其与 5-HT 药物的关系。

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