Pretreatment with 5-HT1A receptor agonist flesinoxan attenuates Fos protein in rat hypothalamus
Pretreatment with 5-HT1A receptor agonist flesinoxan attenuates Fos protein in rat hypothalamus
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DOI：
10.1016/s0014-2999(97)00071-x
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发表时间：
1997-04-18
影响因子：
5
通讯作者：
Olivier, B
中科院分区：
文献类型：
--
作者：
Compaan, JC;Groenink, L;Olivier, B
5-HT 1A受体激动剂flesinoxan具有抗焦虑活性，同时可提高大鼠血浆皮质酮水平。24小时后第二次注射flesinoxan后，皮质酮反应消失，但抗焦虑作用没有消失。雄性大鼠在24小时内接受两次flesinoxan或溶媒注射。Flesinoxan激发增强了Fos免疫反应性下丘脑室旁核，中央杏仁核，和终纹床核的背外侧部分和血浆皮质酮水平的车辆预处理的大鼠。Flesinoxan预处理导致血浆皮质酮水平和Fos阳性神经元在下丘脑室旁核的衰减反应，但在中央杏仁核和床核后flesinoxan的挑战。flesinoxan治疗后的行为和神经内分泌反应的差异脱敏水平似乎对应于大脑中的不同组织水平，如边缘系统和下丘脑。(C)1997年Elsevier Science B.V.
The 5-HT1A receptor agonist flesinoxan has anxiolytic activity and concurrently enhances plasma corticosterone levels in rats. After a second injection of flesinoxan 24 h later, the corticosterone response disappears, but not the anxiolytic effects. Male rats received two injections with either flesinoxan or vehicle within 24 h. Flesinoxan challenge enhanced Fos immunoreactivity in the paraventricular nucleus of the hypothalamus, the central amygdala, and the dorsolateral part of the bed nucleus of the stria terminalis and plasma corticosterone levels in the vehicle-pretreated rats. Flesinoxan pretreatment resulted in an attenuated response of plasma corticosterone levels and Fos-positive neurons in the paraventricular nucleus of the hypothalamus, but not in the central amygdala and the bed nucleus after a flesinoxan challenge. The differential desensitization levels for both behaviour and neuroendocrine responses after flesinoxan treatment seem to correspond to different organization levels in the brain, like limbic system and hypothalamus. (C) 1997 Elsevier Science B.V.