The current model suggests that stage-specific ecdysis behavior is produced by small triggering steps (probably due to other releasing factors, including the neuropeptides corazonin (COR) (Kim et al., 2004) and a diuretic hormone (DH) related to mammalian corticotropin releasing factor (Kim et al., 2006a).
COR and DH release first produce a small amount of ETH release from the peripheral Inka endocrine cells into the blood. ETH starts to act on its central targets, one of which is the pair of EH-producing VM neurons of the brain. ETH-triggered VM cell activity initiates EH release that acts back on the ETH-producing Inka cells to eventually cause a massive ETH release, and finally, this helps cause massive VM release I-BET151 chemical structure of EH (Clark
selleck inhibitor et al., 2004; Ewer and Truman, 1997; Kingan et al., 1997). Ecdysis is a ballistic behavior: it happens infrequently, but it must happen at the correct time; it only lasts for minutes to hours, but cannot be reversed. Its control must therefore be precisely in synchrony with the proper internal state. The precision is due in part to the positive feedback between the two peptide hormone anchors (ETH and EH): this system offers an incremental, processive, and interlocked decision-making mechanism. The final massive release events (that causes release of most ETH and EH stores) are only achieved as the final stage of mutual positive interactions that ensure a timely and proper endocrine resolution and subsequent triggering of behavior. Positive feedback has also been suggested to control ultimate release of neuropeptides that trigger other innate behaviors in insects. Specifically Luan et al. (2012) have analyzed the decision-making network for wing-spreading behavior of newly emerged adult Drosophila that is triggered by the protein hormone bursicon (BUR). BUR is released from a pair of command interneurons (called Bseg) to provoke release of the same hormone from other neurons (called Bag) to support hardening of wing cuticle. The authors infer a loop wherein Bseg activity feeds back positively to permit its own concerted
release of BUR and release of the proper behavioral sequence ( Luan et al., 2012). In endocrinology, ADP ribosylation factor the classic example of a positive feedback system is the control of ovulation in mammals, in which the hypothalamus and ovary interact positively to generate the luteinizing hormone surge that coordinates ovulatory events ( Clarke, 1995). A threshold level of estrogen is reached in the follicular phase of the ovarian cycle and this signals changes from a negative feedback to a positive one: it now activates cells within the brain, probably disinhibiting inhibitory systems and activating positive inputs including kisspetin and noradrenergic afferents to gonadotropin releasing hormone (GnRH) neurons ( Smith et al., 2011).