Reproductive Endocrine Profile of a Strain of Rats Which Exhibits Aspermatogenesis and Reduced Growth1

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Abstract
A line with rats with defects in reproduction (BIL/1 or BY1 strains) was studied to determine whether the defects in spermatogenesis were due to an insufficiency of gonadotropins or steroids. In the aspermatic male, no deficiencies in circulating LH [luteinizing hormone, lutropin], FSH [follicle stimulating hormone, follitropin] or testosterone were observed. The regulatory mechanisms controlling the serum concentrations of these hormones were intact as shown by the ability of the pituitary gland to respond appropriately to a decrease or an increase in circulating testosterone. An androgen-dependent tissue (prostate) was capable of normal metabolism and localization of steroids and no abnormalities were observed in prostate, seminal vesicles or preputial gland when examined histologically. Various cellular components of the testis were capable of binding exogenous gonadotropins and exogenous LH administration resulted in a normal response, as measured by increased testosterone secretion. The normal intratesticular temperature suggested that aspermatogenesis was not due to an abnormally increased testicular temperature. These experiments exclude certain endocrine parameters as the causative agent in this genetically controlled defect in spermatogenesis.

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