Hypothalamic control of gonadotropin release in amphibia: Evidence from studies of gonadotropin release in vitro and in vivo

Abstract

Homogenates of frog ( Rana pipiens) hypothalami stimulated in vitro release of bioassayable LH-like gonadotropin from frog hemipituitaries. In the first of two experiments gonadotropin release was significantly increased 3.7 times by 3.6 hypothalami/ml. In the second experiment 3.6 hypothalami/ml doubled the rate of gonadotropin release, but this increase was not statistically significant. A homogenate of frog neural and intermediate lobes did not increase the rate of gonadotropin release. Frog hypothalamic extract alone had no effect in the bioassay. Synthetic GnRH (Abbott), tested in vitro at 10 and 100 ng/ml each in two experiments, increased the release of gonadotropin between 2.6 and 10 times. Synthetic TRH did not stimulate in vitro release of gonadotropin. One microgram of GnRH injected into the dorsal lymph sac of PMS-pretreated Xenopus laevis caused ovulation in two out of four toads, while 1 μg of GnRH injected three times daily for 4 days into Xenopus with initially regressed ovaries had initiated vitellogenesis in one of two toads when the ovaries were examined after 8 days. In the absence of Ca 2+ in the incubation medium, no stimulatory action of hypothalamic extract or GnRH on gonadotropin release was observed, and in this respect the action of releasing factors on frog gonadotropin release is similar to that on LH release in mammals. High potassium ion levels (5 times normal) stimulated in vitro release of gonadotropin 5.8 times over controls, another observation similar to experimence with mammals. It is concluded that the frog hypothalamus contains a factor capable of causing in vitro release of LH-like gonadotropin from the frog pituitary and that this factor may be similar in nature and mechanism of action to mammalian GnRH, which in frogs is active in vivo and in vitro.