Benech J C, Crispino M, Kaplan B B, Giuditta A
Instituto de Investigaciones Biologicas Clemente Estable, Montevideo, Uruguay.
J Neurosci Res. 1999 Mar 15;55(6):776-81. doi: 10.1002/(SICI)1097-4547(19990315)55:6<776::AID-JNR12>3.0.CO;2-1.
Previous biochemical, autoradiographic, and ultrastructural data have shown that, in the synaptosomal fraction of the squid optic lobe, protein synthesis is largely due to the presynaptic terminals of the retinal photoreceptor neurons (Crispino et al. [1993a] Mol. Cell. Neurosci. 4:366-374; Crispino et al. [1993b] J. Neurochem. 61:1144-1146; Crispino et al. [1997] J. Neurosci. 17:7694-7702). We now report that this process is close to its maximum at the basal concentration of cytosolic Ca++, and is markedly inhibited when the concentration of this ion is either decreased or increased. This conclusion is supported by the results of experiments with: 1) compounds known to increase the level of cytosolic Ca++, such as A23187, ionomycin, thapsigargin, and caffeine; 2) compounds sequestering cytosolic calcium ions such as BAPTA-AM; and 3) agents that block the role of Ca++ as second messenger, such as TFP and W7, which inhibit calmodulin, and calphostin, which inhibits protein kinase C. We conclude that variations in the level of cytosolic Ca++ induced in presynaptic terminals by neuronal activity may contribute to the modulation of the local synthesis of protein.
先前的生化、放射自显影和超微结构数据表明,在鱿鱼视叶的突触体部分,蛋白质合成主要归因于视网膜光感受器神经元的突触前终末(克里斯皮诺等人[1993a]《分子与细胞神经科学》4:366 - 374;克里斯皮诺等人[1993b]《神经化学杂志》61:1144 - 1146;克里斯皮诺等人[1997]《神经科学杂志》17:7694 - 7702)。我们现在报告,这个过程在胞质钙离子的基础浓度时接近其最大值,而当该离子浓度降低或升高时则受到显著抑制。这一结论得到了以下实验结果的支持:1)已知能增加胞质钙离子水平的化合物,如A23187、离子霉素、毒胡萝卜素和咖啡因;2)螯合胞质钙离子的化合物,如BAPTA - AM;3)阻断钙离子作为第二信使作用的试剂,如抑制钙调蛋白的TFP和W7,以及抑制蛋白激酶C的钙磷蛋白。我们得出结论,神经元活动在突触前终末诱导的胞质钙离子水平变化可能有助于调节局部蛋白质合成。