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Short-term sleep deprivation immediately after contextual conditioning inhibits BDNF signaling and disrupts memory consolidation in predator odor trauma mice model of PTSD
Brain Research ( IF 2.9 ) Pub Date : 2020-10-15 , DOI: 10.1016/j.brainres.2020.147155
Rishi Sharma 1 , Pradeep Sahota 1 , Mahesh M Thakkar 1
Affiliation  

Post-traumatic stress disorder (PTSD) is a debilitating neuropsychiatric illness affecting > 7 million people every year in the US. Recently, we have shown that the mouse model of predator odor trauma (POT) displayed contextual conditioning and core features of PTSD including sleep disturbances (hyperarousal) and retrieval of traumatic memories following exposure to objective reminders (re-experiencing). PTSD is a disorder of memory function. Since memory consolidation requires the expression of BDNF along with an activation of MAPK/pERK signaling pathway in limbic brain structures (hippocampus and amygdala) and sleep favors memory consolidation, we hypothesized that short-term sleep deprivation (SD, 3 h), immediately after contextual conditioning will attenuate molecular correlates of memory consolidation, sleep disturbances, and memory consolidation. We performed two experiments in adult male C57BL/6J mice to test our hypothesis. Experiment 1 determined the effects of SD on contextual conditioning and changes in sleep wakefulness. Experiment 2 determined the effects of SD on contextual conditioning-induced changes in the expression of BDNF and pERK in hippocampus and amygdala. SD immediately after contextual conditioning (POT + SD group) significantly attenuated sleep disturbances, memory retrieval, and expression of pERK and BDNF in the hippocampus and amygdala as compared to POT-SD group (no SD after contextual conditioning). No significant differences were observed between POT + SD, NOC-SD (no contextual conditioning + no SD), and NOC + SD (no contextual conditioning + SD) groups. Memory consolidation requires sleep and the expression of pERK and BDNF in hippocampus and amygdala immediately after contextual conditioning in POT model of PTSD in mice.



中文翻译:

在 PTSD 捕食者气味创伤小鼠模型中,情境条件反射后立即短期睡眠剥夺抑制 BDNF 信号并破坏记忆巩固

创伤后应激障碍 (PTSD) 是一种使人衰弱的神经精神疾病,每年在美国影响超过 700 万人。最近,我们已经证明捕食者气味创伤 (POT) 的小鼠模型显示了 PTSD 的情境条件和核心特征,包括睡眠障碍(过度觉醒)和暴露于客观提醒(重新体验)后创伤记忆的恢复。PTSD 是一种记忆功能障碍。由于记忆巩固需要 BDNF 的表达以及边缘脑结构(海马和杏仁核)中 MAPK/pERK 信号通路的激活,并且睡眠有利于记忆巩固,我们假设短期睡眠剥夺(SD,3 小时),在情境条件会减弱记忆巩固、睡眠障碍、和记忆巩固。我们在成年雄性 C57BL/6J 小鼠中进行了两个实验来检验我们的假设。实验 1 确定了 SD 对情境条件和睡眠觉醒变化的影响。实验 2 确定了 SD 对背景条件诱导的海马和杏仁核中 BDNF 和 pERK 表达变化的影响。与 POT-SD 组(情境调节后无 SD)相比,情境调节后立即进行 SD(POT + SD 组)可显着减轻睡眠障碍、记忆恢复以及海马和杏仁核中 pERK 和 BDNF 的表达。在 POT + SD、NOC-SD(无上下文条件反射 + 无 SD)和 NOC + SD(无上下文条件反射 + SD)组之间没有观察到显着差异。

更新日期:2020-10-30
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