Lovinger D M, Colley P A, Akers R F, Nelson R B, Routtenberg A
Brain Res. 1986 Dec 10;399(2):205-11. doi: 10.1016/0006-8993(86)91510-6.
One hour after long-term potentiation (LTP) in the intact hippocampus, a selective increase in protein F1 in vitro phosphorylation was observed in homogenate prepared from dorsal hippocampus. Protein F1 phosphorylation was directly related to the magnitude and persistence of potentiation. No other phosphoprotein studied exhibited a relationship with synaptic enhancement. Low-frequency, non-potentiating stimulation did not increase protein F1 phosphorylation, and phosphorylation of F1 was not elevated when high-frequency stimulation did not produce potentiation. We also confirmed our earlier demonstration of a similar pattern of results 5 min after LTP. In related work we have previously observed: that protein F1 is a substrate for protein kinase C (PKC); that membrane PKC activity was increased by translocation from the cytosol following LTP; and that membrane PKC activity was directly related to the persistence of enhancement. We therefore predicted in the present study that protein F1 phosphorylation in a dorsal hippocampal membrane fraction would be related to LTP. Hippocampal membrane protein F1 was found to be directly related to both the magnitude and persistence of response enhancement. Thus the molecular events leading to prolonged potentiation may involve increased PKC/protein F1 association. Persistence of potentiation may be related to synaptic growth processes involving the growth-associated function of protein F1.
在完整海马体中诱导长时程增强（LTP）一小时后，在取自背侧海马体的匀浆中观察到蛋白质F1的体外磷酸化有选择性增加。蛋白质F1的磷酸化与增强的幅度和持续性直接相关。所研究的其他磷蛋白均未表现出与突触增强的关系。低频、非增强性刺激不会增加蛋白质F1的磷酸化，当高频刺激未产生增强时，F1的磷酸化也不会升高。我们还证实了我们早期的研究结果，即在LTP后5分钟也出现了类似的结果模式。在相关工作中，我们之前观察到：蛋白质F1是蛋白激酶C（PKC）的底物；LTP后，膜PKC活性通过从胞质溶胶转位而增加；并且膜PKC活性与增强的持续性直接相关。因此，我们在本研究中预测，背侧海马体膜部分中的蛋白质F1磷酸化将与LTP相关。发现海马体膜蛋白F1与反应增强的幅度和持续性均直接相关。因此，导致长期增强的分子事件可能涉及PKC/蛋白质F1结合增加。增强的持续性可能与涉及蛋白质F1生长相关功能的突触生长过程有关。
