Ovarian biochemical competence following gonadotrophic deprivation from birth.

Normal ovarian morphogenesis is impaired by the absence of gonadotrophic hormones from birth. In the present study, the following question was asked: Does gonadotrophic deprivation also affect ovarian biochemical competence? Newborn mice were treated daily with an antiserum neutralizing endogenous circulating gonadotrophins. At the age of 14 days, ovaries from these mice and control littermates were incubated in the presence and absence of gonadotrophic preparations; cAMP and lactic acid levels were then measured in tissue and incubation medium. Ovaries from anti-gonadotrophin treated and control mice had the same basal levels, per mg tissue, of cAMP and lactic acid. Moreover, the levels increased to approximately the same extent following in vitro gonadotrophic stimulation: an increase in cAMP of 8-10-fold (using a preparation with an hLH:hFSH ratio of 1:1) or 2 1/2-fold (using a preparation with an hLH:hFSH ratio of 1:5), and about a 2-fold increase in lactic acid (using oLH). The acute effect of gonadotrophins on ovarian glycolysis, reported up till now only in the rat ovary, is the first such demonstration in mice. The results also indicate that despite impaired morphogenesis, the enzymatic systems necessary for ovarian glycolysis (as measured by lactic acid production) and cAMP formation can develop without gonadotrophic participation. Furthermore, ovarian capacity to respond to hormonal stimulation is acquired post-natally, as shown by refractoriness to gonadotrophic stimulation during the first week of life. Finally, post-natal gonadotrophic exposure does not seem an essential requirement, at least as measured by the above parameters, for acquiring ovarian competence to respond to hormonal stimulation.