Nieto-Quero Andrea, Infantes-López María Inmaculada, Zambrana-Infantes Emma, Chaves-Peña Patricia, Gavito Ana L, Munoz-Martin Jose, Tabbai Sara, Márquez Javier, Rodríguez de Fonseca Fernando, García-Fernández María Inmaculada, Santín Luis J, Pedraza Carmen, Pérez-Martín Margarita
Departamento de Psicobiología y Metodología de las Ciencias del Comportamiento, Universidad de Málaga, 29010 Malaga, Spain.
Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina-IBIMA Plataforma Bionand, 29590 Malaga, Spain.
Cells. 2023 Sep 15;12(18):2290. doi: 10.3390/cells12182290.
Intense stress, especially traumatic stress, can trigger disabling responses and in some cases even lead to the development of posttraumatic stress disorder (PTSD). PTSD is heterogeneous, accompanied by a range of distress symptoms and treatment-resistant disorders that may be associated with a number of other psychopathologies. PTSD is a very heterogeneous disorder with different subtypes that depend on, among other factors, the type of stressor that provokes it. However, the neurobiological mechanisms are poorly understood. The study of early stress responses may hint at the way PTSD develops and improve the understanding of the neurobiological mechanisms involved in its onset, opening the opportunity for possible preventive treatments. Proteomics is a promising strategy for characterizing these early mechanisms underlying the development of PTSD. The aim of the work was to understand how exposure to acute and intense stress using water immersion restraint stress (WIRS), which could be reminiscent of natural disaster, may induce several PTSD-associated symptoms and changes in the hippocampal proteomic profile. The results showed that exposure to WIRS induced behavioural symptoms and corticosterone levels reminiscent of PTSD. Moreover, the expression profiles of hippocampal proteins at 1 h and 24 h after stress were deregulated in favour of increased inflammation and reduced neuroplasticity, which was validated by histological studies and cytokine determination. Taken together, these results suggest that neuroplastic and inflammatory dysregulation may be a therapeutic target for the treatment of post-traumatic stress disorders.
强烈的压力,尤其是创伤性压力,会引发使人丧失能力的反应,在某些情况下甚至会导致创伤后应激障碍(PTSD)的发展。PTSD具有异质性,伴有一系列痛苦症状和难治性障碍,这些可能与许多其他精神病理学有关。PTSD是一种非常异质性的疾病,有不同的亚型,这取决于多种因素,包括引发它的应激源类型。然而,其神经生物学机制尚不清楚。对早期应激反应的研究可能会提示PTSD的发展方式,并增进对其发病所涉及的神经生物学机制的理解,为可能的预防性治疗提供机会。蛋白质组学是表征PTSD发展背后这些早期机制的一种有前景的策略。这项工作的目的是了解使用水浸束缚应激(WIRS)暴露于急性和强烈压力下(这可能使人联想到自然灾害)如何诱导几种与PTSD相关的症状以及海马蛋白质组学特征的变化。结果表明,暴露于WIRS会诱导出类似于PTSD的行为症状和皮质酮水平。此外,应激后1小时和24小时海马蛋白的表达谱失调,有利于炎症增加和神经可塑性降低,这通过组织学研究和细胞因子测定得到了验证。综上所述,这些结果表明神经可塑性和炎症失调可能是创伤后应激障碍治疗的一个治疗靶点。