Mira Rodrigo G, Quintanilla Rodrigo A, Cerpa Waldo
Laboratorio de Función y Patología Neuronal, Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontifica Universidad Católica de Chile, Santiago 8331150, Chile.
Centro de Excelencia en Biomedicina de Magallanes (CEBIMA), Universidad de Magallanes, Punta Arenas 6213515, Chile.
Antioxidants (Basel). 2023 Feb 7;12(2):403. doi: 10.3390/antiox12020403.
Traumatic brain injury (TBI) is brain damage due to external forces. Mild TBI (mTBI) is the most common form of TBI, and repeated mTBI is a risk factor for developing neurodegenerative diseases. Several mechanisms of neuronal damage have been described in the cortex and hippocampus, including mitochondrial dysfunction. However, up until now, there have been no studies evaluating mitochondrial calcium dynamics. Here, we evaluated mitochondrial calcium dynamics in an mTBI model in mice using isolated hippocampal mitochondria for biochemical studies. We observed that 24 h after mTBI, there is a decrease in mitochondrial membrane potential and an increase in basal matrix calcium levels. These findings are accompanied by increased mitochondrial calcium efflux and no changes in mitochondrial calcium uptake. We also observed an increase in NCLX protein levels and calcium retention capacity. Our results suggest that under mTBI, the hippocampal cells respond by incrementing NCLX levels to restore mitochondrial function.
创伤性脑损伤（TBI）是指由外力导致的脑损伤。轻度创伤性脑损伤（mTBI）是TBI最常见的形式，反复发生的mTBI是患神经退行性疾病的一个风险因素。在大脑皮层和海马体中，已经描述了几种神经元损伤机制，包括线粒体功能障碍。然而，截至目前，尚无评估线粒体钙动力学的研究。在此，我们使用分离的海马体线粒体进行生化研究，在小鼠mTBI模型中评估线粒体钙动力学。我们观察到，mTBI后24小时，线粒体膜电位降低，基质钙基础水平升高。这些发现伴随着线粒体钙外流增加，而线粒体钙摄取没有变化。我们还观察到NCLX蛋白水平和钙潴留能力增加。我们的结果表明，在mTBI情况下，海马体细胞通过增加NCLX水平来做出反应，以恢复线粒体功能。
