Does corazonin signal nutritional stress in insects?

The undecapeptide corazonin, initially discovered from the American cockroach as a strong cardioaccelerator, is now known to be ubiquitously present in arthropods, although it is absent from some species, notably Coleoptera. The structure of its precursor is similar to the GnRH precursor, while it acts through a receptor related to the GnRH receptor; corazonin thus appears to be an arthropod homolog of GnRH. It is produced by neuroendocrine cells in the brain, as well as interneurons in the ventral nerve cord. These two cell types are generally present in insects; in most species there are also other neurons producing corazonin. Its function in insects has remained obscure; its cardioacceleratory effects are limited to a few cockroach species, while in other species different physiological effects have been described. Most spectacularly it induces changes associated with the gregarious phase in migratory locusts and in the silkworm it reduces the size of the cocoon formed. Corazonin is able to induce ecdysis in two moth species, however locusts and flies in which the corazonin gene is no longer expressed, ecdyse normally and, hence, it is not clear whether corazonin is essential for ecdysis. As the corazonin neuroendocrine cells in the brain express receptors for two midgut peptides, it seems likely that their activity is modulated by the midgut endocrine cells. I propose that in insects corazonin might be released under conditions of nutritional stress, which can explain several of the observed physiological effects of this neurohormone.