Jørgensen M B, Jensen C V, Diemer N H
Pharmabiotec Research Center, University of Copenhagen, Denmark.
Brain Res. 1991 Jan 11;538(2):246-50. doi: 10.1016/0006-8993(91)90436-y.
A quantitative autoradiographic study was made on the binding of the phosphatidylinositol system ligand [3H]inositol(1,4,5)-trisphosphate (IP3) to forebrain sections from rats decapitated various times after 10 min of forebrain ischemia. To investigate the effect of a deafferentation of the hippocampal CA1, kainic acid-induced CA3-lesioned rats with or without 10 min of cerebral ischemia, were also included. The highest binding was found in the hippocampal CA1. Ten min of cerebral ischemia did not change the binding significantly. Between 5 min and 1 h of recirculation there was a 25-35% binding decline in all regions. In the CA1, where the pyramidal cells became necrotic 6 days after ischemia, there was a further decline to 16% of control. In the cortex, where there is no necrosis in this model, binding did not return to control values until day 14. Four days after a selective CA3 lesion with kainic acid, there was a significant 25% decline in the cortex, dentate gyrus and CA1, whereas in the necrotic CA3 binding declined to 54% of control. Ten min of ischemia did not alter this binding significantly. This decrease in calcium mobilizing intracellular receptors after ischemia and seizures could be due to increased membrane degradation, or to a more specific down-regulation following increased intracellular concentration of calcium and IP3.
对磷脂酰肌醇系统配体[3H]肌醇（1,4,5）-三磷酸（IP3）与前脑缺血10分钟后不同时间断头的大鼠前脑切片的结合进行了定量放射自显影研究。为了研究海马CA1区传入神经切断的影响，还纳入了 kainic 酸诱导的CA3损伤大鼠，这些大鼠有或没有经历10分钟的脑缺血。发现海马CA1区的结合最高。10分钟的脑缺血并未显著改变结合情况。在再灌注5分钟至1小时之间，所有区域的结合下降了25%-35%。在CA1区，缺血6天后锥体细胞坏死，结合进一步下降至对照值的16%。在该模型中无坏死的皮质中，结合直到第14天才恢复到对照值。在用 kainic 酸进行选择性CA3损伤4天后，皮质、齿状回和CA1区的结合显著下降25%，而在坏死的CA3区，结合下降至对照值的54%。10分钟的缺血并未显著改变这种结合。缺血和癫痫发作后钙动员细胞内受体的这种减少可能是由于膜降解增加，或者是由于细胞内钙和IP3浓度增加后更特异性的下调所致。
