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.

中文翻译：

---

基底外侧杏仁核而非内侧前额叶皮层有助于慢性氟西汀治疗小鼠 PTSD 症状

在情境提醒阶段，慢性氟西汀治疗是否可以减轻足震引起的创伤后应激障碍 (PTSD) 症状，包括恐惧和共存抑郁症？此外，内侧前额叶皮层 (mPFC) 的子区域，包括扣带回皮层 1 (Cg1)、前缘皮层 (PrL)、下缘皮层 (IL) 和基底外侧杏仁核 (BLA)，参与氟西汀改善 PTSD 症状? 这两个关键问题在本研究中得到了解决。所有小鼠都注射了慢性氟西汀或生理盐水治疗适应（14 天）、足震恐惧条件（1 天）和情境提醒（3 天）阶段。适应后，小鼠接受足部电击（2 mA，10 秒）或非足部电击，并在足部电击箱中停留 2 分钟以进行恐惧调节。之后，在情境提醒阶段，他们被放置在电击箱中 2 分钟。在情境提醒阶段的最后阶段，进行了强迫游泳试验（FST）和免疫组织化学染色。结果表明，足震引起恐惧和共存抑郁症。同时，慢性氟西汀治疗减少了恐惧和抑郁行为。Cg1、PrL、IL 和 BLA 似乎在情境提醒阶段在足震诱导的 PTSD 症状后增加了 c-Fos 表达。氟西汀处理仅降低了 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，包括 Cg1、PrL 和 IL 在内的 mPFC 并未介导因氟西汀引起的 PTSD 症状的改善。