Reactive structural dynamics of synaptic mitochondria in ischemic delayed neuronal death
Reactive structural dynamics of synaptic mitochondria in ischemic delayed neuronal death
复制标题
DOI：
10.1196/annals.1378.003
复制
发表时间：
2006-01-01
期刊：
影响因子：
--
通讯作者：
De Angelis, Clara
中科院分区：
文献类型：
--
作者：
Bertoni-Freddari, Carlo;Fattoretti, Patrizia;De Angelis, Clara
本文观察了短暂性全脑缺血对3月龄大鼠CA1区神经元远端树突突触线粒体超微结构的影响。对年龄匹配的对照组进行假手术。用计算机辅助形态计量学方法测定线粒体数密度(NV)、线粒体平均大小(Average Volume：V)、线粒体长径(Fmax)以及线粒体占据神经细胞的总比例(体积密度：Vv)。与对照组相比，缺血大鼠的NV无显著降低10%，V无显著增加11%，Fmax无显著增加5%。作为这些平衡变化的最终结果，VV在被调查的两个试验组之间保持不变。在缺血动物中，V的百分比分布表明，CA1突触线粒体的群体由较大的细胞器组成，而Fmax分布表明，这种增大是由于延长的细胞器的百分比增加所致。因此，观察到的大小增加不应被认为是一种肿胀现象；相反，它可能代表了线粒体生物发生中的一个生理和有充分证据的步骤。上述参数目前被认为是关于线粒体形态在不同环境刺激下的适应性结构重组的信息。可以想象，这些发现证明了CA1突触终末线粒体结构动力学对缺血的积极反应，并建议将这些细胞器作为开发神经保护性治疗干预措施的可靠靶点，以治疗脑血管疾病，例如中风。
The effect of transient global ischemia on the ultrastructural features of synaptic mitochondria at the distal dendrites of CA1 hippocampal neurons was investigated in 3-month-old rats. Sham surgery was performed on age-matched controls. The number of mitochondria/mu m3 of neurophils (Nv: numeric density), the mitochondrial average size (average volume: V), and longer diameter (Fmax) as well as the overall fraction of neurophils occupied by mitochondria (volume density: Vv) were measured by computer-assisted morphometry. In ischemic rats, a 10% nonsignificant decrease of Nv was found, V increased nonsignificantly by 11%, and Fmax increased nonsignificantly by 5% versus controls. As a final outcome of these balanced changes, Vv remained unchanged between the two experimental groups investigated. In ischemic animals, the percentage distribution of V showed that the population of CA1 synaptic mitochondria was composed by an increased fraction of oversized organelles, while the Fmax distribution revealed that this enlargement was due to an increased percentage of elongated organelles. Thus, the observed increase in size should not be considered as a swelling phenomenon; on the contrary, it may represent a physiological and well-documented step in mitochondrial biogenesis. The above parameters are currently supposed to provide information on the adaptive structural reorganization of mitochondrial morphology under different environmental stimulations. Conceivably, these findings document a positive reactive response to ischemia of the mitochondrial structural dynamics at CA1 synaptic terminals and suggest consideration of these organelles as reliable targets in the development of neuroprotective therapeutic interventions to treat vascular brain diseases, for example, stroke.