Saur Lisiani, Baptista Pedro Porto Alegre, Bagatini Pamela Brambilla, Neves Laura Tartari, de Oliveira Raquel Mattos, Vaz Sabrina Pereira, Ferreira Kelly, Machado Susane Alves, Mestriner Régis Gemerasca, Xavier Léder Leal
Laboratório de Biologia Celular e Tecidual, Departamento de Ciências Morfofisiológicas, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Avenida Ipiranga, 6681, Prédio 12C, Sala 104, Porto Alegre, RS, CEP 90619-900, Brazil.
Neurochem Res. 2016 Apr;41(4):892-904. doi: 10.1007/s11064-015-1770-3. Epub 2015 Nov 17.
Post-traumatic stress disorder (PTSD) is a psychiatric condition resulting from exposure to a traumatic event. It is characterized by several debilitating symptoms including re-experiencing the past trauma, avoidance behavior, increased fear, and hyperarousal. Key roles in the neuropathology of PTSD and its symptomatology have been attributed to the hippocampus and amygdala. These regions are involved in explicit memory processes and context encoding during fear conditioning. The aim of our study was to investigate whether PTSD is capable of altering the morphology, density and expression of glial fibrillary acidic protein (GFAP) in astrocytes from the CA1 region of the hippocampus and the medial amygdala and correlate the data obtained with the orientation index of the polarity of astrocytes. Thirty male rats were divided in two groups: control (n = 15) and PTSD (n = 15). The inescapable shock protocol, in which the animals are exposed to a single episode of footshock, was used to induce PTSD. Our results show that, in the hippocampus, PTSD is capable of decreasing the density of GFAP+ astrocytes as well as altering astrocytic morphology, as shown by the reductions observed in the total number of primary processes, in the number of primary processes in the lateral quadrants, and the degree of branching in the lateral quadrants. The analysis of the orientation index indicates that PTSD alters the polarity of hippocampal astrocytes. No alterations were observed in the amygdala astrocytes. Therefore, this study demonstrates notable changes in hippocampal astrocytes, supporting the concept that these cells play an important role in PTSD symptomatology.
创伤后应激障碍（PTSD）是一种因暴露于创伤性事件而导致的精神疾病。其特征是出现多种使人衰弱的症状，包括再次体验过去的创伤、回避行为、恐惧增加和过度觉醒。海马体和杏仁核在PTSD的神经病理学及其症状学中起着关键作用。这些区域参与了恐惧条件反射过程中的显性记忆过程和情境编码。我们研究的目的是调查PTSD是否能够改变海马体CA1区和内侧杏仁核星形胶质细胞中胶质纤维酸性蛋白（GFAP）的形态、密度和表达，并将获得的数据与星形胶质细胞极性的取向指数相关联。30只雄性大鼠被分为两组：对照组（n = 15）和PTSD组（n = 15）。采用不可逃避电击方案，即让动物暴露于单次足部电击，以诱导PTSD。我们的结果表明，在海马体中，PTSD能够降低GFAP+星形胶质细胞的密度，并改变星形胶质细胞的形态，这表现为初级突起总数、外侧象限初级突起数量以及外侧象限分支程度的减少。对取向指数的分析表明，PTSD改变了海马体星形胶质细胞的极性。在杏仁核星形胶质细胞中未观察到改变。因此，本研究证明了海马体星形胶质细胞有显著变化，支持了这些细胞在PTSD症状学中起重要作用的观点。
