Gene-specific pituitary gland responsiveness of ovariectomized FecB or FecC carrier and non-carrier ewe crosses with German Mutton Merino, Texel and Suffolk breeds to LHRH before and after oestradiol or progesterone treatments

摘要

These studies were undertaken to establish whether there are gene-specific differences in FSH and LH concentrations in the plasma of ovariectomized ewes that are crosses between local breeds (German Mutton Merino, Texel or Suffolk) and carriers and non-carriers of Booroola (FecB) or Cambridge (FecC) genes for prolificacy. The relationships of FSH or LH levels to ovulation rates, predetermined over two oestrus cycles before ovariectomy, were also determined. Ewes that were carriers (F+) or non-carriers (F++) of Booroola or Cambridge genes included in the studies were: Booroola x German Merino (BM), Booroola x Texel (BT), Cambridge x Cambridge (CC), Cambridge x Suffolk (CS) and Cambridge x Texel (CT). Ovulation rates were significantly higher in the F+ genotypes than in the F++ genotypes. Basal and LHRH-induced FSH and LH secretion in ovariectomized ewes were measured in plasma of blood collected by venipuncture. The effects of oestradiol-17beta (E2) or progesterone (P4) implants for 8 days, acting as ovarian feedback hormone, on basal FSH and LH secretion and on pituitary responsiveness to LHRH were also determined. Basal and peak levels of FSH, LH and % responsiveness to LHRH were compared between fecundity genotypes within breeds and between breeds. Basal concentrations of FSH or LH were similar in genotypes within breeds. Both genotypes showed similar responsiveness to LHRH by a significant increase in both FSH and LH secretion. E2 treatment significantly depressed basal FSH and LH secretion; the effect being similar in genotypes within breeds. However, E2 significantly increased pituitary responsiveness to LHRH. P4 only marginally increased basal and LHRH-induced FSH secretion but had no effect on basal LH levels. It significantly increased LHRH-induced LH secretion in FecB but not in FecC ewes. The effect was similar in both genotypes within breeds. No relationships could be established between the concentrations of FSH or LH at basal or peak levels and ovulation rates of the genotypes. BT ewes (F+ and F++) had lower FSH levels than the BM (F+ and F++) as a result of greater sensitivity to E2 and lower responsiveness to LHRH. Consequently, the BT tended to have a lower ovulation rate than the BM. The Cambridge breeds (within genotypes) showed no differences in the levels of basal or LHRH-induced FSH or LH secretion and sensitivities to E2 or P4 were not significantly different. Their ovulation rates were not different either. In conclusion, although both FSH and LH play important roles in follicular development and ovulation, it seems unlikely that the pituitary is a major site for the effects of the FecB and FecC fecundity genes in regulating ovulation rates in heterozygous carriers and in homozygous non-carriers taken from sheep crosses, since there were no gene-specific differences in FSH or LH between fecundity genotypes