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K. K. Schillo, M. A. Green and S. H. Hayes

Summary. Finnish Landrace × Southdown ewes were ovariectomized (OVX) and subjected to daily photoperiods of 16L:8D (Group I) or 8L:16D (Group II) for 84 days. Ewes were then either adrenalectomized (ADX) (N = 5 for Group I; N = 4 for Group II) or sham ADX (N = 6 for Groups I + II). After surgery, ewes in Group I were subjected to 8L:16D for 91 days and 16L:8D for 91 days whereas ewes in Group II were exposed to 16L:8D for 91 days and 8L:16D for 91 days. Oestradiol implants were inserted into all ewes on Day 148. Sequential blood samples were taken at 28, 56, 91, 119, 147 and 168 days after surgery to determine secretory profiles of LH and prolactin. Photoperiod did not influence LH release in Group I in the absence of oestradiol. Although photoperiod influenced frequency and amplitude of LH pulses in Group II before oestradiol treatment, adrenalectomy did not prevent these changes in patterns of LH release. However, in Group II the increase in LH pulse amplitude during exposure to long days was greater (P < 0·01) in adrenalectomized ewes than in sham-operated ewes. Mean concentrations of LH increased in ADX ewes on Days 91 (P = 0·07) and 119 (P < 0·05). Adrenalectomy failed to influence photoperiod-induced changes in mean concentrations of LH, amplitude of LH pulses and frequency of LH pulses in the presence of oestradiol. Concentrations of prolactin were influenced by photoperiod. In Groups I and II concentrations of prolactin increased (P < 0·01) after adrenalectomy, but the magnitude of this effect decreased over time. These results suggest that the effects of photoperiod on patterns of LH release are mediated in part by a mechanism that is not dependent on sex steroids and that the adrenal may influence release of prolactin.

Keywords: photoperiod; LH; prolactin; adrenalectomy; sheep

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P. Licht, T. Hayes, P. Tsai, G. Cunha, H. Kim, M. Golbus, S. Hayward, M. C. Martin, R. B. Jaffe and S. E. Glickman

According to common understanding of sexual differentiation, the formation and development of a penile clitoris in female spotted hyaenas requires the presence of naturally circulating androgens during fetal life. The purpose of the present study was to determine potential source(s) of such fetal androgens by investigating the timing of urogenital development and placental production of androgen during early and mid-gestation. Fetuses determined to be female by molecular techniques (lack of SRY gene) at days 33 and 48 of gestation had undifferentiated gonads, but the clitoris was already 'masculinized' and was generally similar to the phallus of a 50-day-old male fetus. Wolffian and Müllerian ducts terminated at the urogenital sinus in both sexes and a urethra was present along the entire length of the clitoris and penis. The adrenal gland was large and histologically differentiated at 33 days. Steroid gradients across the uterus (a drop in Δ4-androstenedione, with increases in oestrogen and androgen), and high androstenedione in ovarian veins indicated that ovarian androstenedione was metabolized and secreted as testosterone by the placenta throughout gestation. In vitro, whole or homogenized placentae at days 48 and 58 of gestation (110 days total) metabolized radiolabelled androstenedione into testosterone and oestradiol; the specific enzymatic activity of early placental tissues was higher than at later stages. A human placental homogenate had higher aromatase activity but did not produce testosterone unless aromatase was inhibited. Infusion of labelled androstenedione into the uterine arteries of hyaenas demonstrated the conversion of this substrate into testosterone and oestradiol and their secretion into the fetal circulation. Evidently, androgen is produced by the placenta and secreted into the fetal circulation from early in pregnancy when masculinization is first evident, before differentiation of the fetal ovary.