尼莫地平对脑损伤后神经细胞钙通道和超微结构的改变

Effects of Nimodipine on Changes of Neuronal Calcium Channel and Neuronal Ultrastructure following Brain Injury

采用细胞内Ｃａ２＋荧光探针Ｆｕｒａ－２／ＡＭ检测大鼠脑损伤后神经元突触体胞浆中游离Ｃａ２＋浓度（［Ｃａ２＋］ｉ），以研究神经细胞钙通道变化，并选用Ｃａ２＋通道阻断剂尼莫地平治疗，观察神经细胞Ｃａ２＋通道变化和超微结构的改变。结果表明，脑损伤后神经细胞钙通道开放，突触体胞浆中游离［Ｃａ２＋］ｉ在伤后０．５小时即已升高为１．０９±０．０８×１０－６Ｍ／Ｌ水平（Ｐ＜０．００１），伤后６、２４、４８和７２小时，［Ｃａ２＋］ｉ持续处于１０－６Ｍ／Ｌ水平以上。同时发现神经细胞Ｃａ２＋超载时，其超微结构损害。应用尼莫地平治疗后，神经细胞胞浆游离［Ｃａ２＋］ｉ明显下降，超微结构损害显著减轻。

e studied the changes of neuronal calcium channel by detecting concentration of cytosolic free calcium[Ca2+]i of the synap-tosomas of neuronal cells following brain injury in rats.The calcium antagonist. nimodipine was selected to observe its effects onchanges of neuronal calcium channel and neuronal ultrastructure. The reseults showed that the neuron calcium channel opened andinduced the increasing cytosolic free[Ca2+]i after brain injury. The increase of cytosolic free[Ca2+]i within neuronal synaptosomeswas significant(P<0. 001) 0.5h after brain injury. Its value was 1. 09±0. 08×10-6 M/L. The levels of[Ca2+]i Kept at over 10-6M/L at 6, 24, 48 and 72h after brain injury.The disruption of neuronal ultrastructure was due to the calcium overload of neurons. Nimodipine showed the effects of reducing cytosolic free[Ca2+]i and gave an advantage to neuronal damage in this experiment.