Figure 13

Model for regulation of PETH/ETH expression, release and action. Increased ecdysteroid levels induce expression of eth in Inka cells and ethr in the CNS, CA, H-organ, epidermis, Malpighian tubules and other organs. Ecdysteroid decline provides signal to release corazonin from the brain-CC-CA complex that elicits secretion of PETH/ETH from Inka cells. PETH/ETH action on multiple targets in the CNS results in initiation of the consecutive phases of the ecdysis sequence. PETH/ETH activation of ETHR-A neurons producing kinins/DHs leads to initiation of pre-ecdysis I, while ETHR-B neurons producing PDF-like peptide control pre-ecdysis II. About 30 min into pre-ecdysis, increased levels of PETH/ETH activate the ecdysis network which is composed of ETHR-A cells that produce EH in the brain and segmental neurons NS-27 and IN-704 expressing AST-CC, CCAP, MIPs and bursicon in the ventral nerve cord. However, the ecdysis onset is delayed by aminergic inhibitory ETHR-B neurons in the SG and TG1-3 and ETHR-A/B neurons producing AST-A in the AG1-8. After 1 h of pre-ecdysis, segmental interneurons DLT1-3 producing NPF suppress the descending inhibition and evoke central release of AST-CC, CCAP, MIPs and bursicon to initiate the ecdysis behavior. Simultaneously, a mixture of neuropeptides CCH1, CT and MIPs produced by ETHR-A/B neurons PM9 control proctodeal contractions to shed the inner cuticle lining the hindgut. Immediately after the old cuticle is shed, the ecdysis behavior is terminated by the central release of sNPF and MIPs from ETHR-A neurons VL8 in the posterior TAG. ETH/EH-activated network of ETHR-A neurons (NS-27 and IN-704) producing bursicon and other factors control post-ecdysis processes—cuticle plasticization, expansion, sclerotization and pigmentation. PETH/ETH action on its receptors in peripheral organs include air swallowing by the FG, production of JH by the CA, production of biogenic amines from the H-organ and regulation of water balance by MT cells on surface of the Malpighian tubules.