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创伤后应激障碍及相关共病的突触可塑性:诊断和治疗的功能与机制。

Synaptic Plasticity in PTSD and associated Comorbidities: The Function and Mechanism for Diagnostics and Therapy.

机构信息

State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China.

College of Pharmacy and Bioengineering, Chongqing University of Technology, Chongqing 400054, China.

出版信息

Curr Pharm Des. 2018;24(34):4051-4059. doi: 10.2174/1381612824666181120094749.

DOI:10.2174/1381612824666181120094749
PMID:30457048
Abstract

The studying of synaptic plasticity, the ability of synaptic connections between neurons to be weakened or strengthened and specifically long-term potentiation (LTP) and long-term depression (LTD), is one of the most active areas of research in neuroscience. The process of synaptic connections playing a crucial role in improving cognitive processes is important to the processing of information in brain. In general, the dysfunction of synaptic plasticity was involved in a wide spectrum of central nervous system (CNS) disorders, including some neurodegenerative disorders. Thus, synaptic plasticity which is a dysfunction reported in neurodegenerative disorders may also be involved in posttraumatic stress disorder (PTSD), an anxiety and/or memory disorder developed after experiencing natural disasters, domestic violence or combat-related trauma. In this review, we mainly focus on discussing the biological function and mechanism for diagnostics and therapy of synaptic plasticity in PTSD and associated comorbidities, such as schizophrenia, depression, sleep disturbances and alcohol dependence, and further studying the molecular mechanisms of PTSD with a particular focus on the LTP/LTD, glutamatergic ligand-receptor systems, voltage-gated calcium channels (VGCCs) and brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB). The summarized function and mechanism of synaptic plasticity in PTSD and its comorbidities may help us further understand PTSD and provide insight into novel neuroplasticity modifying for diagnostics and treatment for PTSD.

摘要

突触可塑性的研究,即神经元之间突触连接的减弱或增强能力,特别是长时程增强(LTP)和长时程抑制(LTD),是神经科学中最活跃的研究领域之一。突触连接在改善认知过程中起着至关重要的作用,这对大脑信息处理很重要。一般来说,突触可塑性的功能障碍与广泛的中枢神经系统(CNS)疾病有关,包括一些神经退行性疾病。因此,神经退行性疾病中报道的突触可塑性功能障碍也可能与创伤后应激障碍(PTSD)有关,PTSD 是经历自然灾害、家庭暴力或与战斗相关的创伤后出现的焦虑和/或记忆障碍。在这篇综述中,我们主要集中讨论突触可塑性在 PTSD 及相关共病(如精神分裂症、抑郁症、睡眠障碍和酒精依赖)中的诊断和治疗的生物学功能和机制,并进一步研究 PTSD 的分子机制,特别关注 LTP/LTD、谷氨酸能配体-受体系统、电压门控钙通道(VGCCs)和脑源性神经营养因子(BDNF)-酪氨酸激酶 B(TrkB)。总结的突触可塑性在 PTSD 及其共病中的功能和机制,可能有助于我们进一步了解 PTSD,并为 PTSD 的诊断和治疗提供新的神经可塑性修饰的思路。

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