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The aim of this study was to investigate the role of FSH in the control of ovulation rate by the Booroola gene. Three Booroola genotypes (Fec^BFec^B, Fec^BFec⁺ and Fec⁺Fec⁺) of the F₂ population, from a cross between Booroola Merino and Scottish Blackface, and two Booroola genotypes (Fec^BFec⁺ and Fec⁺Fec⁺; 25% Booroola Merino and 75% Scottish Blackface), from the backcross of Fec^BFec⁺ sires to Scottish Blackface ewes, were compared. During seasonal anoestrus significant differences (P < 0.05) in hCG-stimulated ovulation rates were obtained between Fec^BFec^B and Fec⁺Fec⁺ ewes from the F₂ population, and Fec^BFec⁺ ewes were intermediate. No significant difference in hCG-stimulated ovulation rate was observed in the backcross population between Fec^BFec⁺ ewes and Fec⁺Fec⁺ ewes. There were no significant differences between genotypes in mean serum FSH concentrations during seasonal anoestrus in either backcross or F₂ populations. During the breeding season, two separate experiments confirmed the expected ovulation rate differences between genotypes (Fec^BFec^B > Fec^BFec⁺ > Fec⁺Fec⁺). In both experiments, mean peripheral FSH concentrations in the F₂ population were similar in Fec^BFec⁺ and Fec⁺Fec⁺ ewes, but were significantly higher (P < 0.05) in Fec^BFec^B ewes. In the backcross population, mean peripheral FSH concentrations during the oestrous cycle were not significantly different between Fec^BFec⁺ and Fec⁺Fec⁺ ewes, despite significant differences in ovulation rate. Ovariectomy during the breeding season resulted in significantly higher (P < 0.001) mean peripheral FSH concentrations in all three genotypes. After ovariectomy, mean FSH concentrations between Fec^BFec⁺ and Fec⁺Fec⁺ ewes, from both the backcross and F₂ populations, were not significantly different. However, mean FSH concentrations in the F₂ population were significantly higher in Fec^BFec^B ewes than in the other two genotypes. The pattern of differences between genotype in peripheral FSH concentrations and ovulation rates suggest that FSH is not wholly responsible for differences in ovulation rate between genotypes. The results support the hypothesis that the Fec^B gene is operating both within the ovary and at the level of the hypothalamus and pituitary gland.

Summary. A high and a low response line in sheep were selected on the basis of the mean concentration of LH in 10-week-old Finn–Dorset ram lambs after an i.v. injection of 5 μg GnRH. After 8 male generations the mean LH response of the high line was more than 5-fold that of the low line and the heritability of the selected trait was estimated at 0·44 ± 0·015. Highly significant line differences in mean LH response to GnRH were also found in males at 20 weeks of age and females at 10 and 20 weeks of age and the genetic correlations between the four LH response traits appear to be close to unity. Large line differences in the mean FSH response to GnRH were also found in both males and females at 10 and 20 weeks of age. Selection had little effect on the physical characteristics of lambs. High-response line ewes entering their first breeding season at about 7 months of age showed oestrus earlier in the season and had higher ovulation rates and numbers of lambs born per ewe lambing than did low-response line ewes. In the second breeding season, at about 19 months of age, the only line difference was a higher ovulation rate early in the breeding season in high-line ewes. It is suggested that these changes may be mediated by a more rapid response in high-line ewes to increased GnRH stimulation at puberty or at the beginning of the breeding season.

Keywords: genetic selection; LH release; GnRH; sheep

Summary. Harderian glands of Syrian hamsters contained measurable levels of immunoreactive somatostatin. After an extraction procedure, serial dilutions of tissue were assayed and showed parallelism in the displacement curve with dilutions of purified somatostatin standard in the radioimmunoassay. Somatostatin concentrations were higher in female hamsters (10·0 ± 2·1 ng/mg protein) than in males (2·6 ± 0·4 ng/mg protein). Castrated males had somatostatin values in the range of females (12·4 ± 2·3 ng/mg protein) at 1 month after gonadectomy. Testosterone implants prevented the rise of Harderian gland somatostatin in castrated males. Gonadectomized males had lower somatostatin content in the gland than did control males (1·0 ± 0·2 ng/mg protein) at 2 months after castration. Somatostatin values in females were unaffected by gonadectomy, but there were variations during the oestrous cycle, with a nadir dectected at dioestrus-1 and maximal values coincident with the day of the ovulation.

Keywords: somatostatin; Harderian gland; androgens; Syrian hamster

Timely activation of the luteinizing hormone receptor (LHCGR) is critical for fertility. Activating mutations in LHCGR cause familial male-limited precocious puberty (FMPP) due to premature synthesis of testosterone. A mouse model of FMPP (KiLHR^D582G), expressing a constitutively activating mutation in LHCGR, was previously developed in our laboratory. KiLHR^D582G mice became progressively infertile due to sexual dysfunction and exhibited smooth muscle loss and chondrocyte accumulation in the penis. In this study, we tested the hypothesis that KiLHR^D582G mice had erectile dysfunction due to impaired smooth muscle function. Apomorphine-induced erection studies determined that KiLHR^D582G mice had erectile dysfunction. Penile smooth muscle and endothelial function were assessed using penile cavernosal strips. Penile endothelial cell content was not changed in KiLHR^D582G mice. The maximal relaxation response to acetylcholine and the nitric oxide donor, sodium nitroprusside, was significantly reduced in KiLHR^D582G mice indicating an impairment in the nitric oxide (NO)-mediated signaling. Cyclic GMP (cGMP) levels were significantly reduced in KiLHR^D582G mice in response to acetylcholine, sodium nitroprusside and the soluble guanylate cyclase stimulator, BAY 41-2272. Expression of NOS1, NOS3 and PKRG1 were unchanged. The Rho-kinase signaling pathway for smooth muscle contraction was not altered. Together, these data indicate that KiLHR^D582G mice have erectile dysfunction due to impaired NO-mediated activation of soluble guanylate cyclase resulting in decreased levels of cGMP and penile smooth muscle relaxation. These studies in the KiLHR^D582G mice demonstrate that activating mutations in the mouse LHCGR cause erectile dysfunction due to impairment of the NO-mediated signaling pathway in the penile smooth muscle.