Moult cycle‐related changes in biological activity of moult‐inhibiting hormone (MIH) and crustacean hyperglycaemic hormone (CHH) in the crab, Carcinus maenas

Abstract

The currently accepted model of moult control in crustaceans relies entirely on the hypothesis that moult-inhibiting hormone (MIH) and crustacean hyperglycaemic hormone (CHH) repress ecdysteroid synthesis of the target tissue (Y-organ) only during intermoult, and that changes in synthesis and/or release of these neurohormones are central to moult control. To further refine this model, we investigated the biological activities of these neuropeptides in the crab Carcinus maenas, at the target tissue, receptor and cellular level by bioassay (inhibition of ecdysteroid synthesis), radioligand (receptor) binding assays, and second messenger (cGMP) assays, at defined stages of the moult cycle. To investigate possible moult cycle-related changes in neuropeptide biosynthesis, steady-state transcript levels of both neuropeptide mRNAs were measured by quantitative RT-PCR, and stored neuropeptide levels in the sinus gland were quantified during intermoult and premoult. The results show that the most important level of moult control lies within the signalling machinery of the target tissue, that expression and biosynthesis of both neuropeptides is constant during the moult cycle, and are not central to the currently accepted model of moult control.

Roles of crustacean hyperglycaemic hormone in ionic and metabolic homeostasis in the Christmas Island Blue crabDiscoplax celeste

“…In recent years, a variety of other functions for these hormones have been established, involving (for example) inhibition of ecdysteroid (Webster and Keller, 1986;Chang et al, 1990;Chung and Webster, 2003;Chung and Webster, 2005), methyl farnesoate (Liu et al, 1997) and ovarian protein synthesis (Khayat et al, 1998;Avarre et al, 2001). A subject of topical interest is the involvement of CHH in ionoregulatory processes (Charmantier-Daures et al, 1994;Charmantier et al, 1999;Chung et al, 1999;Townsend et al, 2001;Serrano et al, 2003;Chung and Webster, 2006).…”

Nitric oxide production and sequestration in the sinus gland of the green shore crab, Carcinus maneas

“…As MIH transcript levels remain constant over the molt cycle, MIH synthesis and secretion are regulated by post-transcriptional mechanisms (Chung and Webster, 2003) (our unpublished observations). NO inhibits neuropeptide release in the hippocampus, bovine chromaffin cells, basal forebrain and nucleus accumbens in the mammalian brain (Sequeira et al, 1997;Schwarz et al, 1998;Philippu and Prast, 2001).…”

“…mRNA levels of MIH and crustacean hyperglycemic hormone (CHH) in the ESG remain unchanged throughout the molt cycle in Carcinus maenas, indicating that MIH and CHH are regulated post-transcriptionally (Chung and Webster, 2003) (our unpublished observations). The MIH neurons in the XO/SG complex are under serotonergic control (Rudolph and Spaziani, 1991) and neuropeptide release is triggered by entry of Ca 2+ (Cooke, 1985).…”

Endocrine regulation of the reproduction in crustaceans: Identification of potential targets for toxicants and environmental contaminants

“…However, the study with the crab Carcinus maenas L., 1758 demonstrated that the sensitivity of Y-organ itself to MIH is a more important factor than levels of MIH (Chung & Webster 2003). This was also supported by a study with prawn Macrobrachium rosenbergii De Man, 1879, where female eyestalk ablation resulted in shortening of the reproduction molting period but levels of ecdysteroid (as well as vitellogenin) did not substantially vary during molting stages (Okumura & Aida 2001).…”

“…Consequently, regulation of the sensitivity of Y-organ to MIH seems to have an important role. In fact, it has been shown that sensitivity of Y-organ to MIH significantly dropped in the premolt stage, and it was restored again during later molt and postmolt stages, but the factor that modulates the perceptivity of Y-organ has not been described (Chung & Webster 2003). Factors such as alterations in cellular second messengers (cAMP), modulations of steroidogenic enzymes or cholesterol uptake into Y-organ were suggested to be involved (Spaziani et al 1999).…”