Harris R A, Fenner D, Leslie S W
Life Sci. 1983 Jun 6;32(23):2661-6. doi: 10.1016/0024-3205(83)90358-2.
Several physiological stimuli, including neuronal depolarization, increase the production of phosphatidate (PA) from phosphatidylinositol (PI) and increase calcium fluxes across cell membranes. To determine if breakdown of PI is required for neuronal calcium uptake, we tested inhibitors of PI-specific phospholipase C on depolarization-dependent uptake of calcium by isolated brain synaptosomes. At a concentration of 0.1 mM these inhibitors reduced calcium uptake produced by depolarization for 1 to 3 sec, but did not affect uptake due to more prolonged depolarization. Exogenous PA also stimulated calcium accumulation by synaptosomes and this uptake was not reduced by the enzyme inhibitors. These results suggest that the rapid calcium influx produced by neuronal depolarization may be mediated by the breakdown of PI.
包括神经元去极化在内的几种生理刺激，会增加磷脂酸（PA）从磷脂酰肌醇（PI）的生成，并增加跨细胞膜的钙通量。为了确定PI的分解对于神经元摄取钙是否必要，我们测试了PI特异性磷脂酶C抑制剂对离体脑突触体去极化依赖性钙摄取的影响。在浓度为0.1 mM时，这些抑制剂在去极化1至3秒时减少了钙摄取，但不影响因更长时间去极化导致的摄取。外源性PA也刺激了突触体的钙积累，并且这种摄取并未被酶抑制剂所减少。这些结果表明，神经元去极化产生的快速钙内流可能由PI的分解介导。
