Effects of Postpubertal Ovarian Steroids on Reproductive Function and Sexual Differentiation of Lightly Androgenized Rats*

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Abstract
To determine the possible role of ovarian steroids in the development of sterility in lightly androgenized rats that exhibit the delayed anovulation syndrome (DAS), rats were ovariectomized prepubertally and the ability of steroids to facilitate LH [luteinizing hormone] secretion was tested before and after prolonged treatment with oil, estradiol benzoate (EB), or testosterone propionate (TP). The LH response of the animals was compared to that of additional androgenized rats ovariectomized after onset of sterility, as well as to rats given oil neonatally. Female rats given oil (normals) or 10 .mu.g TP (DAS) at 5 days of age were either ovariectomized at 30 days or left intact until 95 days. Rats ovariectomized prepubertally were given EB at 1000 h on day 32, and bled for RIA [radioimmunoassay] of plasma LH at 24, 31, and 55 h after EB. Daily injections of oil, EB, or TP were given to the ovariectomized rats for 60 days, beginning on day 35. A blood sample was taken at the end of the injections, and intact rats were ovariectomized at that time. One month later, a blood sample was taken and EB was injected and followed 72 h later by progesterone (P). Blood samples were taken 29 and 53 h after EB and 5 h after P. Compared to DAS rats, normal rats responded to EB at 32 days with higher LH values at 31 and 55 h after EB. Chronic treatment with EB or TP inhibited LH secretion, but LH values had returned to the level of the oil-injected controls when EB was injected in the second LH facilitation test. Although the response to P in this second test was unaltered by any adult treatment in normal rats, DAS rats given oil chronically had higher LH values 5 h after P than did rats given EB or TP for 60 days or sterile rats ovariectomized at 95 days. Prepubertal ovariectomy followed by chronic oil treatment prevented the loss of the ability of P to facilitate LH secretion that occurred in intact or spayed and steroid-treated rats. Lordosis behavior after EB plus P and after EB only was tested beginning 3 and 5 wk, respectively, after the LH facilitation test. There were no differences among any of the groups in the lordotic response to P, but androgenized rats had overall higher lordosis behavior scores after EB only. These data suggest that in lightly androgenized rats, postpubertal ovarian secretions, perhaps estrogen and/or testosterone, may play a role in the development of refractoriness to the facilitatory effects of P on LH secretion, but do not alter the ability of steroids to induce sexual behavior.