Abstract
As in other teleosts, the completion of oogenesis is crucial for the acquisition of reproductive maturity in female freshwater eels. However, freshwater eels have a unique migratory lifecycle, which means that natural reproductive development can only be researched up until early vitellogenesis. Following this, a captivity-induced reproductive block must be overridden by external treatment with pituitary homogenates to stimulate artificial maturation. Artificial maturation of eels remains relatively inefficient when compared to other teleosts. This is partially due to a lack of knowledge pertaining to how mediators of the hypothalamic-pituitary-gonadal axis such as sex steroids and gonadotropins regulate reproductive development. These hormones interact with specific receptors to affect change in target cells.
This study aimed to determine the effects of combined or separate treatments with estradiol-17β (E2), 11-ketotestosterone (11KT) or human chorionic gonadotropin (hCG) on reproductive development in the New Zealand shortfinned eel, Anguilla australis. To achieve this, in vivo experiments were executed to evaluate the effect of treatments with or without 11KT ± hCG and 11KT ± E2 on ovarian development and the gene expression of pituitary and ovarian hormone receptors. Androgen and estrogen receptor subtypes (ars, ers; a and b subtypes) were differentially regulated in the ovary and pituitary in response to hormones. Both 11KT and hCG regulated the expression of ars and ers in the pituitary and ovary whereas E2 only stimulated era expression in the pituitary. Similarly, 11KT and hCG both reduced the expression of follicle-stimulating hormone beta in the pituitary while stimulating the expression of follicle-stimulating hormone receptor in the ovary. Independently, 11KT increased oocyte size and E2 stimulated hepatic production of vitellogenin (VTG). However, co-treatment with 11KT and E2 achieved uptake of VTG into oocytes. Additionally, hCG effectively induced vitellogenesis in the early pubertal eel.
Overall, this research confirmed that hCG is an effective stimulator of vitellogenesis while also mediating hormone receptor expression, potentially sensitising the pituitary and ovary to circulating hormones. From these results, it was also speculated that through receptor mediation, 11KT might sensitize the ovary to sex steroids and follicle-stimulating hormone during early development and in turn facilitate the incorporation of E2-induced VTG into the developing oocyte. These results highlighted the potential of sex steroid co-treatments to induce vitellogenesis in eels even in the absence of external gonadotropin treatment.