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Effect of acute immunoneutralization of inhibin in ewes during the late luteal phase of the oestrous cycle on ovarian hormone secretion and follicular development during the subsequent follicular phase

Ewes with ovarian autotransplants received either inhibin antiserum (10 ml i.v.; n = 6) or sheep serum (10 ml i.v.; n = 5) on day 10 of the luteal phase with additional daily injections (1 ml i.v.) from 48 h after the initial injection until the end of blood sampling, 9 days later. Luteal regression was induced by injection of prostaglandin F₂ (PGF₂) 4.2 days after the initial plasma injection. Jugular and ovarian venous blood samples were taken every 4 h over the experimental period, and more frequent samples (every 10–15 min for 2–3 h) were taken to examine pulsatile secretory responses from the ovary to GnRH-induced (150 ng i.m. 1 and 4 days after initial treatment) or endogenous LH pulses (24 and 48 h after injection of PGF₂). Plasma FSH concentrations, ovarian steroid secretion and ovarian follicular development were measured. Immunization against inhibin resulted in a two- to threefold increase (P < 0.001) in plasma FSH concentrations, which remained higher than controls until injection of PGF₂. Within 24 h of immunization, there was an increase in the number of small ovarian follicles (P < 0.01) and by 4 days after treatment, immunized ewes had four or five (P < 0.01) large ovarian follicles and, despite little change in the basal steroid secretion, a four- to sixfold increase (P < 0.05) in the amplitude of the steroidogenic response to a GnRH-induced LH pulse. After induction of luteolysis, basal oestradiol and androstenedione secretion increased markedly to a preovulatory peak three- to fivefold higher (P < 0.01) than that of controls and occurring 24 h earlier (P < 0.001). As a result, the time of the preovulatory LH surge was also advanced 24 h in immunized ewes (P < 0.001). Induction of luteal regression by injecting PGF₂ resulted in a decrease in FSH concentrations in both treatment groups, but this decrease was more marked in immunized animals (50% of value before PGF₂ was given; P < 0.001) than in controls (20% of value before PGF₂ was given; P < 0.05), so that by 16 h after PGF₂ injection, FSH values were no longer significantly different in the two treatment groups. This large fall in FSH concentrations had no deleterious effects on steroid secretion or the number of large follicles in immunized ewes and, as shown by a marked increase in ovarian size and a threefold increase (P < 0.001) in progesterone concentration during the subsequent luteal phase, these animals had multiple ovulations. We conclude that oestradiol alone can modulate FSH within physiological limits in the absence of inhibin negative feedback during the follicular phase and that the increase in ovulation rate that occurs after inhibin immunization is not caused by attenuation of the follicular phase suppression in FSH.

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