Neuroendocrine regulation of gonadotrophin II release and gonadal growth in the goldfish, Carassius auratus.

Abstract

The goldfish, a member of the carp family, is a widely used model for reproductive neuroendocrine studies of economically important fish. The two gonadotrophin (GTH) molecules released from the fish anterior pituitary, GTH-I and GTH-II, are structurally similar to tetrapod FSH and LH, respectively. Gonadotrophin II is the best studied, and in goldfish stimulates gonadal growth and steroidogenesis, ovulation and sperm release. Growth hormone also has gonadotrophic actions in fish which enhance gonadal steroidogenesis. The principal stimulatory and inhibitory systems regulating GTH-II release are the gonadotrophin-releasing hormone (GnRH) and dopamine neurones in the preoptic-hypothalamic region. In goldfish there are two native GnRH forms, salmon GnRH and chicken GnRH-I; both stimulate GTH-II release but use different signal transduction pathways. In contrast to mammals, teleost fish do not have a median eminence and the GTH-II cells are thus directly innervated by neurones producing GnRH, dopamine and other stimulatory neurohormones. For most of these factors, the ability to stimulate GTH-II release varies seasonally. The amino acid neurotransmitter, gamma-aminobutyric acid, has the most prominent stimulatory actions which enhance GnRH release and inhibit dopamine turnover in the hypothalamo-pituitary complex. Neuropeptide Y stimulates GTH-II release by a combined direct action on the gonadotroph and also by enhancing GnRH release. Positive and negative sex steroid feedback mechanisms act concurrently to regulate GTH-II release in adults of both sexes. The principal site of positive feedback is the GTH-II cell where testosterone and oestradiol potentiate GnRH-stimulated GTH-II release. Negative feedback by sex steroids involves activation of inhibitory dopamine neurones, thus maintaining tight control over circulating GTH-II concentrations.