Effects of fluoxetine on the amygdala and the hippocampus after administration of a single prolonged stress to male Wistar rates: In vivo proton magnetic resonance spectroscopy findings

Effects of fluoxetine on the amygdala and the hippocampus after administration of a single prolonged stress to male Wistar rates: In vivo proton magnetic resonance spectroscopy findings
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DOI:
10.1016/j.pscychresns.2015.02.011
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发表时间:
2015-05-30
影响因子:
2.3
通讯作者:
Shi, Yuxiu
Shi, Yuxiu
中科院分区:
医学4区
文献类型:
--
作者:
Han, Fang;Xiao, Bing;Shi, Yuxiu

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创伤后应激障碍(PTSD)是一种基于焦虑和记忆的障碍。海马体和杏仁核是情绪调节的关键区域。氟西汀被发现可以改善PTSD患者的焦虑相关症状。然而,很少有研究直接研究氟西汀对海马体和杏仁核的影响。在本研究中,雄性Wistar大鼠接受氟西汀或车辆后,暴露于一个单一的长期压力(SOS),创伤后应激障碍的动物模型。在SOS后-1,1,4,7和14天进行在体质子磁共振波谱(H-1-MRS)检查氟西汀对杏仁核、海马和丘脑神经代谢物变化的影响。SOS增加N-乙酰天冬氨酸(NAA)/肌酸(Cr)和胆碱部分(Cho)/Cr的比率在双侧杏仁核的第4天,降低NAA/Cr的比率在左侧海马粘土1,并增加这两个比率在右侧海马第14天。丘脑无明显变化。氟西汀治疗纠正了第4天杏仁核和第14天海马中NAA/Cr和Cho/Cr水平的SPS增加,但未能使第1天左侧海马中与SPS相关的NAA/Cr水平降低正常化。上述结果提示,SOS的发生与杏仁核和海马的代谢异常有关,氟西汀对SOS引起的杏仁核和海马代谢异常的纠正作用不同。这些发现对氟西汀治疗PTSD有一定意义。(C)2015爱思唯尔爱尔兰有限公司版权所有。
Posttraumatic stress disorder (PTSD) is an anxiety- and memory based disorder. The hippocampus and amygdala are key areas in mood regulation. Fluoxetine was found to improve the anxiety-related symptoms of PTSD patients. However, little work has directly examined the effects of fluoxetine on the hippocampus and the amygdala. In the present study, male Wistar rats received fluoxetine or vehicle after exposure to a single prolonged stress (SOS), an animal model of PTSD. In vivo proton magnetic resonance spectroscopy (H-1-MRS) was performed -1, 1,4, 7 and 14 days after SOS to examine the effects of fluoxetine on neurometabolite changes in amygdala, hippocampus and thalamus. SOS increased the N-acetylaspartate (NAA)/creatine (Cr) and choline moieties (Cho)/Cr ratios in the bilateral amygdala on day 4, decreased the NAA/Cr ratio in the left hippocampus on clay 1, and increased both ratios in the right hippocampus on day 14. But no significant change was found in the thalamus. Fluoxetine treatment corrected the SPS increases in the NAA/Cr and Cho/Cr levels in the amygdala on day 4 and in the hippocampus on day 14, but it failed to normalise SPS-associated decreases in NAA/Cr levels in the left hippocampus on day 1. These results suggested that metabolic abnormalities in the amygdala and the hippocampus were involved in SOS, and different effects of fluoxetine in correcting SPS-induced neurometabolite changes among the three areas. These findings have implications for fluoxetine treatment in PTSD. (C) 2015 Elsevier Ireland Ltd. All rights reserved.