In this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na+/K+ pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate.
We discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na+/K+ ATPase elicits SD. Elevated K+ or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling.
Finally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory.
在这篇评论中,我们引入SD作为一个单一或重复的事件,在失去血流后的灰质中产生,这损害了Na+/K+泵。每次SD事件的电恢复需要如此多的能量,以至于神经元通常在初始损伤后数分钟和数小时内死亡。独立于细胞外谷氨酸。
我们讨论了如何在许多实验准备中对SD进行各种陷阱的研究,Na+/K+ATP酶过重如何引起SD。升高的钾或谷氨酸不太可能是SD的天然激活剂。然后我们转向SD本身的属性,专注于它的启动和传播以及计算机建模。
最后,我们总结了作者之间的共识和争论点,以及SD研究可能的方向。在随附的评论中,我们批评谷氨酸兴奋毒性理论的作用,它是如何塑造SD研究的,与SD理论相比,它对早期脑损伤研究的重要性值得怀疑。