The insect molt culminates with ecdysis, a vital behavior that is used to shed the remains of the old cuticle. Ecdysis includes several behavioral subroutines and physiological events that are expressed sequentially to loosen and then shed the old cuticle, then expand and harden the new one. Work on a variety of insects has shown that ecdysis is triggered by the neuropeptide, Ecdysis-Triggering Hormone (ETH), which activates sequentially a number of peptidergic neurons, all of which express the ETH receptor (ETHR), and include neurons that produce Eclosion Hormone, Crustacean Cardioactive Peptide (CCAP), and bursicon, amongst others.

To understand how the complex ecdysial sequence is controlled we have used Drosophila to investigate the consequences on ecdysis behavior of disabling specific neurohormones and their receptors. We have also examined the responses of the corresponding peptidergic neurons and of motoneurons to ETH challenges in vitro, by using a calcium sensitive GFP to monitor the resulting patterns of neural activation.

Our results reveal that the actions of neurohormones downstream of ETH together with GABA-mediated inhibitory actions configure the network’s response to ETH. The resulting patterns of neural activity then control the ensuing sequence of behavioral subroutines.

Our findings contribute to the further understanding of how ecdysis behavior is controlled, and provide insights for understanding how neuropeptides can fundamentally alter the output of a neural network. We will also discuss these findings in light of the fact that ecdysial neurohormones and their receptors are extremely conserved, yet can play different roles in the control of ecdysis between different developmental stages and in different insects.