1. Главная
  2. Ресурсы
  3. Библиотечный поиск
Nitric oxide impairsmitochondrialmovement in corticalneurons duringhypoxia Santina ZanelliPatricia A. TrimmerNina J. Solenski2006 год

Nitric oxide impairs mitochondrial movement in cortical neurons during hypoxia
статья из журнала

Полный текстСтраница публикацииПубликация в OpenAlex
Аннотация: Abstract Cortical nitric oxide (NO) production increases during hypoxia/ischemia in the immature brain and is associated with both neurotoxicity and mitochondrial dysfunction. Mitochondrial redistribution within the cell is critical to normal neuronal function, however, the effects of hypoxia on mitochondrial dynamics are not known. This study tested the hypothesis that hypoxia impairs mitochondrial movement via NO‐mediated pathways. Fluorescently labeled mitochondria were studied using time‐lapse digital video microscopy in cultured cortical neurons exposed either to hypoxia/re‐oxygenation or to diethyleneamine/nitric oxide adduct, DETA‐NO (100–500 µ m ). Two NO synthase inhibitors, were used to determine NO specificity. Mitochondrial mean velocity, the percentage of movement (i.e. the time spent moving) and mitochondrial morphology were analyzed. Exposure to hypoxia reduced mitochondrial movement to 10.4 ± 1.3% at 0 h and 7.4 ± 1.7% at 1 h of re‐oxygenation, versus 25.6 ± 1.4% in controls ( p < 0.05). Mean mitochondrial velocity (µm s −1 ) decreased from 0.374 ± 0.01 in controls to 0.146 ± 0.01 at 0 h and 0.177 ± 0.02 at 1 h of re‐oxygenation ( p < 0.001). Exposure to DETA‐NO resulted in a significant decrease in mean mitochondrial velocity at all tested time points. Treatment with N G ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME) prevented the hypoxia‐induced decrease in mitochondrial movement at 0 h (30.1 ± 1.6%) and at 1 h (26.1 ± 9%) of re‐oxygenation. Exposure to either hypoxia/re‐oxygenation or NO also resulted in the rapid decrease in mitochondrial size. Both hypoxia and NO exposure result in impaired mitochondrial movement and morphology in cultured cortical neurons. As the effect of hypoxia on mitochondrial movement and morphology can be partially prevented by a nitric oxide synthase (NOS) inhibitor, these data suggest that an NO‐mediated pathway is at least partially involved.
Год издания: 2006
Авторы: Santina Zanelli, Patricia A. Trimmer, Nina J. Solenski
Издательство: Wiley
Источник: Journal of Neurochemistry
Ключевые слова: Neonatal and fetal brain pathology, Traumatic Brain Injury and Neurovascular Disturbances, Mitochondrial Function and Pathology
Другие ссылки: Journal of Neurochemistry (PDF)
Journal of Neurochemistry (HTML)
PubMed (HTML)