Influence of GABA on Gonadotrophin Release in the Goldfish

Abstract

The influence of GABA on pituitary gonadotrophin (GTH) release in the goldfish was studied by means of in vivo and in vitro techniques. It was found that GABA injected intraperitoneally caused an increase of serum GTH levels in regressed or early maturing fish, but not in late maturing animals. Moreover, injection of a GABA transaminase inhibitor caused a significant increase of GABA within the hypothalamus and pituitary, and a dose-dependent increase in serum GTH levels. To determine if this effect could be exerted directly at the level of the pituitary, dispersed pituitary cells in static incubation or in perifusion were exposed to increasing concentrations of GABA or its agonists muscimol and baclofen. None of these drugs was able to modify the spontaneous or GnRH-induced secretion of GTH, indicating that the in vivo effect of GABA was most likely mediated via another hypothalamic factor. Using in vitro incubation of pituitary slices, it was found that GABA caused a dose-related stimulation of GnRH release at the level of the pituitary, providing a possible explanation for the observed in vivo stimulatory effect of GABA on GTH release. Since the seasonal effect of GABA in vivo indicated a possible interaction of GABA with sexual steroids, GABA was given intraperitoneally to female goldfish implanted with either testosterone or estradiol. We found that the stimulatory effect of GABA on GTH release was abolished in estradiol-treated females but was still observed in testosterone-implanted fish. Moreover, estradiol but not testosterone caused a decrease of the GABA concentration within the telencephalon. Taken together, these data indicate that GABA is involved in the regulation of GTH secretion in the goldfish, possibly by stimulating the release of GnRH from the pituitary, an effect that appeared to be modulated by estrogens. The inhibitory effects of estrogens on GABA actions may be part of the mechanism of estrogen negative feedback on the brain-pituitary axis.

The effects of bicuculline (a GABAA receptor antagonist) on LHRH-A and pimozide stimulated gonadotropin (GtH2) release in female carp (Cyprinus carpio L.)

“…It is confirmed by recent in vitro and in vivo experiments by Kah et al (1992) and SIoley et al (1992) in which the indirect effect of GABA on GtH2 secretion by influence via dopaminergic neurons is suggested. It is specially important in the case of GABA interaction with a DA-ergic system, which inhibits GtH2 secretion in fish (for review, see Peter et al, 1986).…”

“…As was shown in goldfish by Kah et al (1992) GABA has no direct effect on the gonadotrophs, because there were no effects of GABA on GtH release from dispersed pituitary cells, either in static incubation or in cell column perifusion. In the case of in vitro incubation of pituitary slices, containing both GABA and GnRH terminals, stimulatory effects of GABA on GnRH release were observed.…”

“…It is specially important in the case of GABA interaction with a DA-ergic system, which inhibits GtH2 secretion in fish (for review, see Peter et al, 1986). Recent papers by Roelants et al (1990) and Kah et al (1992) on the in vivo treatment of carp and goldfish with GABA or its agonists present contradictory results. Because of that, the present study was undertaken in two consecutive spawning seasons in order to determine the role of GABA (using bicuculline, a GABAA receptor antagonist) in GtH2 release from the pituitary gland of female carp injected with LHRH analogue and pimozide (PIM) (D 2 receptor antagonist).…”

Steroid effects on the in vitro LH secretion from pituitary cells of sexually immature carp (Cyprinus carpio L.) under the influence of naltrexone and morphine

“…Sex steroids may act directly at the level of the pituitary gland or indirectly via other neurons: GABAergic, serotoninergic, opioid, which in turn affect dopaminergic (inhibitory) and/or GnRH (stimulatory) systems controlling LH secretion and release (Somoza et al, 1988;Rosenblum and Peter, 1989;Kah et al, 1992). Data on the role of opioid peptides in the control of gonadotropin secretion in fish are not abundant (see Introduction) and the relation of opioids to other endocrine factors which ultimately determine blood LH levels is not clear yet.…”

Oestrogen-induced androgen insufficiency results in a reduction of proliferation and differentiation of spermatogonia in the zebrafish testis

“…These data indicate that E 2 inhibited the Gnrh/ Gnrh-receptor signalling system, and that these effects apparently overrule the direct, stimulatory effects of oestrogens on gonadotropin subunit expression. Also signalling pathways towards GnRH neurons, like g-aminobutyric acid (Kah et al 1992), or the recently described Kiss1/Gpr54 system (Elizur 2009) may be influenced by estrogens in teleost fish. Therefore, E 2 -induced gonadotropin insufficiency seems the main factor contributing to the observed downregulation of androgen production in the zebrafish testis, which in turn results in an interruption of spermatogenesis.…”