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. 2015 Sep 24;11(9):e1005513. doi: 10.1371/journal.pgen.1005513

Fig 7. A model depicting functional roles of kinin and CAMB neurons in scheduling of the ecdysis FAP.

Fig 7

ETH release from Inka cells activates ETHR neurons (ETHR-A and ETHR-B). ETHR-B neurons are more sensitive to ETH and become active immediately following ETH release. These neurons release signal(s) that engage Gαo signaling in CAMB neurons. ETH activates kinin neurons directly governing pre-ecdysis and CAMB neurons via ETHR-A and Gαq signaling. Initially, pre-ecdysis is induced, whereas CAMB neurons remain silent due to relatively low sensitivity to ETH and Gαo-mediated inhibitory input. Upon reaching adequate ETH levels in the hemolymph, ETH-mediated Gαq signaling overrides Gαo signaling in CAMB neurons, leading to co-release of CCAP, AstCC, MIP, and bursicon. This results in pre-ecdysis inhibition and the switch to ecdysis behavior and post-ecdysis behavior. Additional excitatory inputs from non-CAMB CCAP neurons contribute to vigorous ecdysis swings, resulting in head eversion. The dashed arrow represents hypothetical input to CAMB neurons from as yet unidentified ETHR-B neurons.