Reproductive hormones modulate differentially brain and ovarian vasotocin receptor gene expression in early and late recrudescent catfish, Heteropneustes fossilis

Abstract

Investigations on the role of the reproductive hormones on VT receptor gene expression are lacking in teleosts. Previously we reported that gonadotropin and steroid hormones modulate the secretion and gene expression of brain and ovarian vasotocin (VT) in the catfish Heteropneustes fossilis. In continuation, in the present study we investigated the role of estradiol-17β (E2), the maturation-inducing steroid (MIS) 17α, 20β-dihydroxy-4-pregnen-3-one (17, 20β-DP), and human chorionic gonadotropin (hCG) on the expression of VT receptor genes (v1a1, v1a2 and v2a) in the brain and ovary of the catfish in early (previtellogenic, preparatory) and late (post vitellogenic, prespawning) phases of the ovarian cycle. The steroid treatments (in vivo and in vitro) modulated only the v1a1 and v1a2 expression in both tissues, but not the v2a expression. The E2-induced modulation of the v1a1 and v1a2 gene expression varied with the reproductive phase. In the preparatory phase, E2 up regulated the expression of brain and ovarian v1a1 and v1a2 gene expression, the response varied with the dose and duration. In the prespawning phase, E2 inhibited the expression in a dose- and duration-dependent manner. On the other hand, 17, 20β-DP up regulated the expression of brain and ovarian v1a1 and v1a2 in both phases, and the response was higher in the prespawning phase and varied with dose and duration. In contrast to the steroid effects, the hCG treatment modulated the expression of all the VT receptor genes only in the prespawning phase and the response varied with dose and duration. The results indicate differential modulatory roles of steroid hormones and hCG on the VT receptor gene expression, to mediate VT’s reproductive or osmoregulatory functions. While the hCG effect on v1a type receptor expression may be steroid- dependent, that of v2a expression seems to be steroid-independent.