Department of Psychology, Fo Guang University, Yilan County 26247, Taiwan.
Department of Biotechnology and Animal Science, National Ilan University, Yilan County 26247, Taiwan.
Behav Neurol. 2020 Nov 25;2020:8875087. doi: 10.1155/2020/8875087. eCollection 2020.
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.
慢性氟西汀治疗是否会减轻情景性提示阶段的足部电击诱导的创伤后应激障碍（PTSD）症状，包括恐惧和共病性抑郁？此外，内侧前额叶皮层（mPFC）的各个亚区，包括扣带皮层 1（Cg1）、额前皮质（PrL）、下边缘皮质（IL）和外侧杏仁核（BLA），是否参与了氟西汀对 PTSD 症状的改善？本研究旨在解决这两个关键问题。所有小鼠均接受慢性氟西汀或生理盐水治疗，用于适应（14 天）、足部电击恐惧条件反射（1 天）和情景提示（3 天）阶段。适应后，将小鼠置于足部电击（2 mA，10 秒）或非足部电击环境下，并在足部电击箱中停留 2 分钟，进行恐惧条件反射。之后，它们在情景提示阶段被放置在足部电击箱中 2 分钟。在情景提示阶段的最后一次实验中，进行强迫游泳测试（FST）和免疫组织化学染色。结果表明，足部电击可引起恐惧和共病性抑郁。同时，慢性氟西汀治疗可减轻恐惧和抑郁行为。在情景性提示阶段足部电击诱导 PTSD 症状后，Cg1、PrL、IL 和 BLA 的 c-Fos 表达似乎增加。氟西汀治疗仅减少了 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，mPFC 包括 Cg1、PrL 和 IL 并没有介导氟西汀改善 PTSD 症状。本研究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。
