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  • Little is known about the endocrinological control


    Little is known about the endocrinological control of reproduction in polychaetes. In vertebrates, gonadal maturation is regulated by the hypothalamo-pituitary-gonadal axis. GnRH, GTHs, and steroid hormones are involved in this axis (see Okubo and Nagahama, 2008). In two polychaete species, Perinereis cultrifera and Neanthes arenaceodentata, cholesterol, which is a precursor of steroid hormones, has been found (Zeeck et al., 1994; Lee et al., 2005). Furthermore, it has been reported that estrogen regulates vitellogenin synthesis in Nereis virens (García-Alonso et al., 2006). Vitellogenin, which is the precursor of yolk protein, is secreted by specialized coelomic EGTA called eleocytes, which is then corporated into the oocytes and stored as vitellin. Taken together, these observations suggest that a steroid hormone is involved in ovarian maturation in polychaetes. Recently, it has been reported that in polychaete Platynereis dumerilii, a neurohormone, which is thought to be GTH, is present in the supra-oesophageal ganglion of mature females and promotes oocyte growth (Lawrence and Soame, 2009). Considering that GTH regulates steroid hormone secretion in vertebrates, it is likely that this neurohormone promotes oocyte growth by stimulating steroid hormones. Moreover, it would be interesting to examine the relationship of mwGnRH and the neurohormone in the cerebral ganglion in future. In summary, we showed the distribution of mwGnRH-ir cell bodies and fibers in the nerve ganglion of the polychaete annelid, Perinereis aibuhitensis, using a newly produced anti-mwGnRH antibody. Our results indicate that mwGnRH is synthesized in the cerebral ganglion, is transported through the subpharyngeal ganglion and the ventral nerve cord, and functions either as a neurotransmitter or neuromodulator. Further studies are necessary to clarify the precise physiological function of mwGnRH in annelids.
    Conclusions The distribution of mwGnRH-ir cell bodies and fibers in the nerve ganglion of the clam worm Perinereis aibuhitensis was clarified by immunohistochemistry. mwGnRH-ir cell bodies were detected in the cerebral ganglion and mwGnRH-ir fibers were widely observed in the optic neuropil, the central neuropil region, the subpharyngeal ganglion, and the ventral nerve cord, suggesting that mwGnRH plays a physiological role in the nervous system of this polychaete annelid.
    Authors’ contributions
    Funding This study was supported in part by a Grant-in-Aid for Scientific Research (B) (No. 20380115) to M.A. from the Ministry of Education, Culture, Sports, Science and Technology, Japan.
    Conflict of interest
    GnRH and GnRH Receptors
    GnRH in the Neuroendocrine Control of Female Reproductive Functions
    The GnRH/GnRHR System in Peripheral Female Reproductive Tissues
    GnRH Analogs in Reproduction Native GnRH has a half-life of 2–4min mainly due to the degradation of the glycine–leucine bond between amino acids 6 and 7. To overcome this limitation, a number of synthetic GnRH analogs have been designed to be used to either restore fertility in patients with GnRH deficiency or suppress the pituitary–gonadal axis. Synthetic GnRH-a generally have a modification in Gly6, usually replaced by a d-amino acid, to increase their plasma half-life, a deleted Gly10-amide and the addition of a residue (ethylamide) to Pro9 to increase the affinity for GnRHRs (Conn & Crowley, 1994; Engel & Schally, 2007). On the other hand, they preserve the amino acid sequence of the N-terminal and the C-terminal domains which are crucial for receptor binding (both N- and C-terminal domains) and activation (N-terminal domain). Fig. 1 reports the mostly used GnRH-a in clinical trials. Pulsatile administration of GnRH-a can be used to stimulate the pituitary–gonadal axis in substitution of native GnRH. However, a prolonged administration of GnRH-a induces an initial stimulation of the pituitary GnRHR and of gonadotropin secretion (flare effect) followed by a receptor downregulation and reproductive axis desensitization resulting in the suppression of gonadotropins and gonadal steroid hormone secretion (medical castration) (Clayton, 1989; Kaiser et al., 1997).