Eclosion hormone-stimulated cGMP levels in the central nervous system of Manduca sexta: inhibition by lipid metabolism blockers, increase in inositol(1,4,5)trisphosphate and further evidence against the involvement of nitric oxide

• Published in: Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology Vol. 165; no. 6; pp. 417 - 427
• Main Authors: Morton, D.B, Simpson, P.J
• Format: Journal Article
• Language: English
• Published: Germany 1995
• Subjects: Animals; bacterial toxins; Carbon Monoxide - metabolism; central nervous system; cyclic GMP; Cyclic GMP - metabolism; Dose-Response Relationship, Drug; enzyme inhibitors; fatty acids; Fatty Acids - pharmacology; GTP-Binding Proteins - metabolism; Hydrolysis; Inositol 1,4,5-Trisphosphate - metabolism; inositol phosphates; Insect Hormones - administration & dosage; Insect Hormones - antagonists & inhibitors; Insect Hormones - pharmacology; ionomycin; ionophores; lipase inhibitors; lipid metabolism; Lipoprotein Lipase - antagonists & inhibitors; Manduca; Manduca sexta; Moths - metabolism; neurohormones; neuropeptides; nitric oxide; Nitric Oxide - antagonists & inhibitors; Nitric Oxide - metabolism; Pertussis Toxin; Protease Inhibitors - pharmacology; regulation; Type C Phospholipases - metabolism; Virulence Factors, Bordetella - pharmacology
• ISSN: 0174-1578; 1432-136X
• DOI: 10.1007/BF00261295

Previous studies have shown that the neuropeptide, eclosion hormone, stimulates a nitric oxide-independent increase in the levels of cGMP in the nervous system of Manduca sexta. By contrast, recent results in Bombyx mori suggest that eclosion hormone increases cGMP via the production of nitric oxide. In view of these conflicting results we have carried out additional studies to test whether nitric oxide is involved in this process in Manduca. Evidence presented here supports our earlier observations that in Manduca the eclosion hormone-stimulated increase in cGMP is nitric oxide- and carbon monoxide-independent. In addition, we show that a wide variety of inhibitors of lipid metabolism block the eclosion hormone-stimulated cGMP increase. This supports the hypothesis that the activation of the guanylate cyclase is mediated by a lipid messenger. We also show that eclosion hormone stimulates an increase in the levels of inositol(1,4,5)trisphosphate. The time-course of this increase is consistent with the hypothesis that eclosion hormone stimulation of a phospholipase C is an early event in the cascade that results in an increase in cGMP. Receptor-mediated lipid hydrolysis is often mediated by G protein-coupled receptors. Experiments using pertussis toxin show that the eclosion hormone-stimulated increase in cGMP is not mediated by a pertussis toxin-sensitive G protein.