Berry R W
Brain Res. 1986 Nov;387(2):185-7. doi: 10.1016/0169-328x(86)90009-4.
Previous studies on the biosynthesis of the peptide egg-laying hormone (ELH) of Aplysia have suggested that the increase in cAMP levels associated with the initiation of a bag cell discharge stimulated ELH synthesis, whereas the calcium influx associated with the discharge inhibits it. This report provides additional documentation of the inhibitory role of calcium. Inhibition by the calcium ionophore A23187 was shown to be dependent on the presence of extracellular calcium. A23187 inhibited ELH synthesis and exposure to 0 Ca2+/2 mM EGTA medium stimulated it in bag cell somata surgically deprived of their sites of synaptic input. The tumor-promoting phorbol ester, TPA, inhibited ELH biosynthesis in a calcium-dependent fashion, whereas the non-tumor-promoting 4 alpha-phorbol did not. These results are consistent with the hypothesis that calcium entry during bag cell discharge may inhibit ELH synthesis via activation of protein kinase C, thus counteracting the stimulation by cAMP early in the discharge. Such a mechanism could precisely regulate the production of ELH molecules to replace those lost by secretion.
先前对海兔产卵激素(ELH)生物合成的研究表明,与套细胞放电起始相关的cAMP水平升高刺激了ELH合成,而与放电相关的钙内流则抑制了它。本报告提供了钙抑制作用的更多证据。钙离子载体A23187的抑制作用被证明依赖于细胞外钙的存在。在手术切除了突触输入部位的套细胞胞体中,A23187抑制ELH合成,而暴露于0 Ca2+/2 mM EGTA培养基中则刺激了ELH合成。促肿瘤的佛波酯TPA以钙依赖的方式抑制ELH生物合成,而非促肿瘤的4α-佛波醇则没有这种作用。这些结果与以下假设一致:套细胞放电期间的钙内流可能通过激活蛋白激酶C来抑制ELH合成,从而抵消放电早期cAMP的刺激作用。这样一种机制可以精确调节ELH分子的产生,以替代因分泌而损失的分子。