Lazarewicz J W
Department of Neurochemistry, Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
Acta Neurobiol Exp (Wars). 1996;56(1):299-311. doi: 10.55782/ane-1996-1135.
The involvement of calcium ions in mechanisms of ischemic brain injury has been suggested for several years. Our understanding of the role of intracellular Ca2+ as a trigger of acute neurotoxicity and in the induction of long lasting processes leading to necrotic and/or apoptotic postischemic delayed neuronal death or of compensatory, neuroprotective mechanisms has increased considerably. Still many questions concerning the generation of Ca+ signal such as the nature of the main routes of ischemic Ca2+ influx to neurones, involvement of intracellular Ca2+ stores and Ca2+ buffers, spatial and temporal relations between ischemia-induced increases in intracellular Ca2+ concentration and neurotoxicity remain open. Some conclusions from experiments in cultured neurones concerning glutamate-evoked destabilization of Ca2+ homeostasis and neurotoxicity may be not relevant to in vivo ischemic conditions. This review, apart from emphasising generally proposed mechanisms of Ca2+ transients and toxicity in ischemic neurones, will discuss some of these controversial issues.
钙离子参与缺血性脑损伤机制的观点已提出数年。我们对细胞内Ca2+作为急性神经毒性触发因素以及在导致缺血后坏死和/或凋亡性延迟神经元死亡的长期过程诱导中，或在代偿性神经保护机制中的作用的理解有了显著提高。然而，关于Ca+信号产生的许多问题仍然悬而未决，例如缺血性Ca2+流入神经元的主要途径的性质、细胞内Ca2+储存和Ca2+缓冲剂的参与、缺血诱导的细胞内Ca2+浓度升高与神经毒性之间的时空关系。一些在培养神经元中进行的实验得出的关于谷氨酸诱发的Ca2+稳态破坏和神经毒性的结论，可能与体内缺血情况无关。本综述除了强调普遍提出的缺血神经元中Ca2+瞬变和毒性机制外，还将讨论其中一些有争议的问题。
