Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health, Bethesda, Maryland, USA.
Nat Neurosci. 2012 Oct;15(10):1359-61. doi: 10.1038/nn.3204. Epub 2012 Sep 2.
Alcoholism is frequently co-morbid with post-traumatic stress disorder, but it is unclear how alcohol affects the neural circuits mediating recovery from trauma. We found that chronic intermittent ethanol (CIE) impaired fear extinction and remodeled the dendritic arbor of medial prefrontal cortical (mPFC) neurons in mice. CIE impaired extinction encoding by infralimbic mPFC neurons in vivo and functionally downregulated burst-mediating NMDA GluN1 receptors. These findings suggest that alcohol may increase risk for trauma-related anxiety disorders by disrupting mPFC-mediated extinction of fear.
酒精中毒常与创伤后应激障碍共病,但目前尚不清楚酒精如何影响介导创伤后恢复的神经回路。我们发现,慢性间歇性乙醇(CIE)会损害小鼠的恐惧消退,并重塑内侧前额叶皮质(mPFC)神经元的树突分支。CIE 在体内损害了扣带前皮质神经元的消退编码,并在功能上下调了爆发介导的 NMDA GluN1 受体。这些发现表明,酒精可能通过破坏 mPFC 介导的恐惧消退,增加与创伤相关的焦虑障碍的风险。