The Actions of Ecdysis Triggering Hormone on the Ventral Nerve Cord of the Hornworm, Manduca sexta


Meeting Abstract

P1.103  Jan. 4  The Actions of Ecdysis Triggering Hormone on the Ventral Nerve Cord of the Hornworm, Manduca sexta EL SHAWA, H*; FUSE, M; San Francisco State University; San Francisco State University hanishawa@sbcglobal.net

In the tobacco hornworm, Manduca sexta, the shedding of the outer cuticle is an extremely important process in the survival of the animal. This process is known as ecdysis and occurs after each molt to allow for continued growth and development. The inability of the animal to shed its cuticle properly makes the animal vulnerable to the environment and predation. The process of ecdysis is regulated by a cascade of hormones. The model for this regulation proposes that Ecdysis Triggering Hormone (ETH) from peripheral glands triggers the release of Eclosion Hormone (EH) from the brain. EH then stimulates the increase of cGMP leading to the release of Crustacean Cardioactive Peptide (CCAP), which ultimately initiates the ecdysis behaviors. ETH, however, has also been shown to activate ecdysis behaviors in vitro directly on the ventral nerve cord in the absence of the brain (Zitnan and Adams, 2000) suggesting that EH is not necessary to initiate the ecdysis cascade. This has suggested a role for ETH as a direct ecdysis trigger. We have found that ETH is sufficient to initiate ecdysis behaviors directly on the ventral nerve cord in vitro, by electrophysiological studies of ecdysis motor patterns in brainless CNS preparations. We have determined that the frequency of burst patterns in brainless preparations is not significantly different from those noted in intact nerve cords, for five of six time points taken. Immunohistochemical staining for cGMP in brainless preparations incubated with ETH shows little to no staining, suggesting that cGMP is not necessary for activation of cells of the VNC. This data suggests that the brain and EH play a smaller role then initially believed in the regulation of the initiation of ecdysis. It also suggests that ETH is not acting via CCAP neurons to initiate ecdysis, or that it acts through a different second messenger system.

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