恐惧反应的"不"时间:在PTSD中可能涉及与氧化相关的机制
Mariana G Fronza1, Bruna F Ferreira1, Isabela Pavan-Silva1
1Pharmacology Departament, Ribeirão Preto Medical School, University of São Paulo, São Paulo 14049-900, Brazil.
Molecules (Basel, Switzerland)
|January 11, 2024
概括
创伤后应激障碍 (PTSD) 涉及神经递质功能的改变. 本综述探讨了氧化 (NO) 和其翻译后修饰 (PTMs) 如何影响压力,恐惧和PTSD.
科学领域:
- 神经科学是一个神经科学.
- 精神病学是一个精神病学.
- 分子生物学分子生物学
背景情况:
- 创伤后应激障碍 (PTSD) 与神经递质系统,特别是谷氨酸的改变有关.
- 压力会影响谷氨酸信号传递,影响突触可塑性和记忆形成.
- 涉及PSD95,nNOS和NOS1AP的N-甲基-D-酸盐受体 (NMDAR) 综合体对于神经元信号传递至关重要.
研究的目的:
- 审查氧化 (NO) 和其翻译后修饰 (PTMs) 在PTSD病理生理学的作用.
- 了解压力,恐惧处理和PTSD中NO信号之间的相互作用.
- 要突出与压力和PTSD相关的NO调节通路.
主要方法:
- 文献综述侧重于NO和PTM在压力和PTSD中的作用.
- 涉及谷氨酸,NMDAR,nNOS和NO的分子通路的分析.
- 检查NO在恐惧获取和灭绝中的参与.
主要成果:
- nNOS/NOS1AP复合体与PTSD易感性和并发性疾病有关.
- NO在恐惧获取和灭绝过程中起作用.
- NO诱导PTM如S-化和化,改变了与细胞内信号相关的蛋白质功能.
结论:
- 了解NO的作用和PTM对于理解PTSD的维持和进展至关重要.
- 在应激反应和PTSD中,NO介导的信号通路具有重要意义.
- 需要对NO诱导的PTM进行进一步的研究,以澄清它们在PTSD病理生理学中的具体作用.
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