Girgenrath S, Smith W A
Department of Biology, Northeastern University, Boston, MA 02115, USA.
Insect Biochem Mol Biol. 1996 May;26(5):455-63. doi: 10.1016/0965-1748(96)00001-x.
Ecdysteroidogenesis in the prothoracic glands of the tobacco hornworm Manduca sexta is stimulated by the cerebral neuropeptide prothoracicotropic hormone (PTTH). PTTH-stimulated cAMP synthesis and ecdysone secretion are dependent on the presence of extracellular calcium, suggesting that PTTH enhances calcium entry into the cytosol. Such entry into the cytosol might involve the opening of a plasma membrane calcium channel, or a mechanism dependent upon prior inositol triphosphate (IP3)-mediated release of intracellularly stored calcium. In pupal prothoracic glands, PTTH does not increase IP3 or other inositol phosphates over-times ranging from seconds up to 30 min, even in the presence of lithium. However, the L-type calcium channel antagonist nitrendipine completely prevents PTTH-stimulated ecdysone synthesis. A 41 kDa G-protein in prothoracic glands is ADP-ribosylated by pertussis toxin. However, PTTH-stimulated ecdysone synthesis is unaffected by prior exposure to pertussis toxin, indicating that the 41 kDa protein is not involved in the acute stimulation of steroidogenesis. By contrast, cholera toxin has a stimulatory effect on ecdysone secretion suggesting the involvement of a Gs-like protein. Based on the absence of PTTH-stimulated inositol phosphate formation in pupal prothoracic glands, it is suggested that calcium mobilization may occur through the opening of a calcium channel, possibly regulated by Gs.
烟草天蛾（Manduca sexta）前胸腺中的蜕皮甾体生成受到脑源神经肽促前胸腺激素（PTTH）的刺激。PTTH刺激的环磷酸腺苷（cAMP）合成和蜕皮激素分泌依赖于细胞外钙的存在，这表明PTTH增强了钙进入细胞质的过程。这种进入细胞质可能涉及质膜钙通道的开放，或者一种依赖于先前由三磷酸肌醇（IP3）介导的细胞内储存钙释放的机制。在蛹期前胸腺中，即使存在锂，PTTH在长达30分钟的时间内也不会使IP3或其他肌醇磷酸增加。然而，L型钙通道拮抗剂尼群地平完全阻止了PTTH刺激的蜕皮激素合成。前胸腺中的一种41 kDa G蛋白被百日咳毒素进行ADP核糖基化。然而，PTTH刺激的蜕皮激素合成不受先前接触百日咳毒素的影响，这表明41 kDa蛋白不参与类固醇生成的急性刺激。相比之下，霍乱毒素对蜕皮激素分泌有刺激作用，提示存在一种类似Gs的蛋白参与其中。基于蛹期前胸腺中不存在PTTH刺激的肌醇磷酸形成，有人提出钙动员可能通过钙通道的开放发生，可能受Gs调节。
