Basolateral Amygdala but Not Medial Prefrontal Cortex Contributes to Chronic Fluoxetine Treatments for PTSD Symptoms in Mice.
Basolateral Amygdala but Not Medial Prefrontal Cortex Contributes to Chronic Fluoxetine Treatments for PTSD Symptoms in Mice.
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基底外侧杏仁核，但没有内侧前额叶皮质有助于小鼠PTSD症状的慢性氟西汀治疗。
DOI：
10.1155/2020/8875087
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发表时间：
2020
影响因子：
2.8
通讯作者：
Huang ACW
中科院分区：
文献类型：
--
作者：
Yu YH;Ou CY;Shyu BC;Huang ACW
长期氟西汀治疗是否可以在情景提醒阶段减少足部休克引起的创伤后应激障碍 (PTSD) 症状，包括恐惧和共病抑郁症？此外，内侧前额叶皮层 (mPFC) 的子区域，包括扣带皮层 1 (Cg1)、前边缘皮层 (PrL)、下边缘皮层 (IL) 和基底外侧杏仁核 (BLA)，是否参与氟西汀改善 PTSD 症状？本研究解决了这两个关键问题。所有小鼠均注射慢性氟西汀或生理盐水治疗，用于适应（14天）、足部电击恐惧调节（1天）和情景提醒（3天）阶段。适应后，对小鼠进行足部电击（2mA，10秒）或非足部电击，并在足部电击箱中停留2分钟以进行恐惧条件反射。随后，在情景提醒阶段将他们放入足部电击箱中2分钟。在情景提醒阶段的最后阶段，进行强迫游泳试验（FST）和免疫组化染色。结果表明，足部电击会引起恐惧和共病抑郁症。与此同时，长期氟西汀治疗减少了恐惧和抑郁行为。在情景提醒阶段，足部电击诱发的 PTSD 症状后，Cg1、PrL、IL 和 BLA 似乎会增加 c-Fos 表达。氟西汀治疗仅降低 BLA 的 c-Fos 表达。研究结果表明，BLA 有助于氟西汀改善 PTSD 症状；然而，mPFC，包括 Cg1、PrL 和 IL，并不能介导氟西汀引起的 PTSD 症状的改善。目前的数据可能有助于我们进一步了解氟西汀治疗 PTSD 症状的神经机制。
Do chronic fluoxetine treatments reduced footshock-induced posttraumatic stress disorder (PTSD) symptoms, including fear and comorbid depression, in the situational reminder phase? Moreover, are the subareas of the medial prefrontal cortex (mPFC), including the cingulate cortex 1 (Cg1), prelimbic cortex (PrL), infralimbic cortex (IL), and basolateral amygdala (BLA), involved in the fluoxetine amelioration of PTSD symptoms? These two crucial issues were addressed in the present study. All mice were injected with chronic fluoxetine or normal saline treatments for the adaptation (14 days), footshock fear conditioning (1 day), and situational reminder (3 days) phases. After adaptation, the mice were subjected to footshock (2 mA, 10 seconds) or nonfootshock and stayed 2 min in a footshock box for 2 min for fear conditioning. Later, they were placed in the footshock box for 2 min in the situational reminder phase. In the final session of the situational reminder phase, a forced swimming test (FST) and immunohistochemical staining were conducted. The results indicated that footshock induced fear and comorbid depression. Meanwhile, chronic fluoxetine treatments reduced fear and depression behaviors. The Cg1, PrL, IL, and BLA were seemingly to increase c-Fos expression after footshock-induced PTSD symptoms in the situational reminder phase. The fluoxetine treatments reduced only the BLA's c-Fos expression. The findings suggest that BLA contributes to the fluoxetine amelioration of PTSD symptoms; however, the mPFC, including the Cg1, PrL, and IL, did not mediate PTSD symptoms' amelioration stemming from fluoxetine. The present data might help us to further understand the neural mechanism of fluoxetine treatments in PTSD symptoms.
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影响因子：
2.3
作者：
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通讯作者：
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