Krystal John H, Abdallah Chadi G, Averill Lynette A, Kelmendi Benjamin, Harpaz-Rotem Ilan, Sanacora Gerard, Southwick Steven M, Duman Ronald S
Department of Psychiatry, Yale University School of Medicine, 300 George St., Suite #901, New Haven, CT, 06511, USA.
Clinical Neuroscience Division, VA National Center for PTSD, VA Connecticut Healthcare System, West Haven, CT, USA.
Curr Psychiatry Rep. 2017 Aug 26;19(10):74. doi: 10.1007/s11920-017-0829-z.
Studies of the neurobiology and treatment of PTSD have highlighted many aspects of the pathophysiology of this disorder that might be relevant to treatment. The purpose of this review is to highlight the potential clinical importance of an often-neglected consequence of stress models in animals that may be relevant to PTSD: the stress-related loss of synaptic connectivity.
Here, we will briefly review evidence that PTSD might be a "synaptic disconnection syndrome" and highlight the importance of this perspective for the emerging therapeutic application of ketamine as a potential rapid-acting treatment for this disorder that may work, in part, by restoring synaptic connectivity. Synaptic disconnection may contribute to the profile of PTSD symptoms that may be targeted by novel pharmacotherapeutics.
创伤后应激障碍（PTSD）的神经生物学及治疗研究突显了该障碍病理生理学中许多可能与治疗相关的方面。本综述的目的是强调动物应激模型中一个常被忽视的后果的潜在临床重要性，该后果可能与PTSD相关：应激相关的突触连接丧失。
在此，我们将简要回顾PTSD可能是一种“突触断开综合征”的证据，并强调这一观点对于氯胺酮作为该障碍潜在快速起效治疗方法的新兴治疗应用的重要性，氯胺酮可能部分通过恢复突触连接起作用。突触断开可能导致PTSD症状特征，而这些症状可能是新型药物治疗的靶点。
