Norepinephrine in Graafian follicles is depleted by follicle-stimulating hormone.

The purpose of the present study was to measure norepinephrine (NE) in Graafian follicles and correlate changes in its concentration with circulating gonadotropins secreted endogenously or administered exogenously. Graafian follicles were removed from the ovaries of adult cycling rats. The follicles were pooled in groups of 10-13, and NE was determined by high performance liquid chromatography. Follicular NE(picograms per micrograms protein) did not change between 0900 h (3.61 +/- 0.34) and 1300 h (3.12 +/- 0.25) on proestrus, but was reduced significantly to 1.45 +/- 0.16 at 2100 h, which is 4 h after the peak of the gonadotropin surge. There was a further reduction to 0.83 +/- 0.08 in fresh corpora lutea taken on estrus at 0900 h. The decrease in follicular NE was prevented in estrous rats which were either hypophysectomized 24 h previously or treated with sodium pentobarbital at 1330 h on proestrus. To determine which pituitary hormone was responsible for follicular NE depletion, rats were injected at 0900 h on proestrus with LH (5 micrograms), FSH (20 micrograms), LH plus FSH (5 and 20 micrograms, respectively), or PRL (20 micrograms), and follicular NE was determined 4 h later. FSH reduced follicular NE significantly to 1.86 +/- 0.16 compared to both the control (3.12 +/- 0.25) and the PRL-injected group (2.92 +/- 0.32), whereas LH caused a small but nonsignificant decrease (2.49 +/- 0.2). Both LH and FSH doses used resulted in ovulation, as determined by counting tubal ova 12 h after hormonal treatment. We conclude that 1) NE in Graafian follicles is markedly reduced within 4 h after the preovulatory gonadotropin surge in the normal cycling rat; this reduction is prevented when the surge is abolished; 2) the hormone responsible for follicular NE depletion is FSH rather than LH or PRL; and 3) finally, it is suggested that follicular NE may be involved with the formation and/or functioning of the corpus luteum.

Follicles explanted from pentobarbitone-treated rats provide a model for atresia.

Graafian follicles from rats treated for 1 or 2 days with pentobarbitone sodium (Nembutal) were similar in appearance to pro-oestrous preovulatory follicles, but after 3 or 4 days of treatment early atretic changes were recognized. Ovulatory efficiency decreased to 88, 70, 52 and 31% after 1, 2, 3 and 4 days of treatment, respectively. The mean +/- s.e.m. rate of accumulation (ng/follicle/24 h) of progesterone, androstenedione and oestradiol was 3.6 +/- 0.7, 4.0 +/- 0.3 and 18.9 +/- 3.9 respectively in preovulatory follicles and 10.2 + 1.7, 0.9 +/- 0.1 and 1.9 +/- 0.4 respectively in follicles explanted from rats treated for 4 days with Nembutal. Addition of LH (5 micrograms/ml) to the culture medium stimulated steroid accumulation by both types of follicles. Thus atretic follicles are characterized by impaired androgen and oestradiol formation. Addition of testosterone (1 microgram/ml) to the culture medium increased the accumulation of oestradiol by atretic follicles. It is inferred that the early stages of atresia of rat follicles are distinguished by a deficiency in the activity of enzymes responsible for the conversion of progesterone to androgens that can serve as substrates for aromatization.

Effect of PMSG on follicular atresia in the immature rat ovary.

Administration of PMSG to 26-day-old rats did not increase the total number (non-atretic and atretic) of preantral (Type 4) and antral (Types 5 and 6) follicles but changed the proportion between non-atretic and atretic follicles. By 12 h after PMSG administration only 7% of Type 5 follicles were atretic, and no atretic follicles of Type 6 were observed, as compared to 52 and 62% atretic follicles, respectively, in the saline-treated controls. PMSG did not decrease the percentage of atresia in preantral (Type 4) follicles. The treatment was associated with a sharp fall by 12 h in the pyknotic index of antral (Types 5 and 6) follicles. It is concluded that PMSG causes superovulation in the rat by rescuing follicles of Types 5 and 6 from atresia and allowing them to reach ovulation.

Estradiol-17 beta reduces number of ovulations in adult rats: direct action on the ovary?

The specific role of estrogen and other steroids in folliculogenesis is unclear since both inhibitory and stimulatory effects have been described. We reported that atresia of the preovulatory follicle was induced when estradiol-17 beta (E2) or progesterone was administered peripherally in rhesus monkeys, presumably due to a direct effect at the ovarian level. The present study was designed to determine if a similar direct action of E2 and other steroids occurs in rats. Minicapsules of Silastic containing E2, progesterone or dihydrotestosterone in amounts of 12.5% to 100% mixed with cholesterol, were placed unilaterally under the ovarian bursa on the morning of metestrus in rats having 4-day cycles. At autopsy on the morning of estrus, the number of oocytes ovulated from treated and untreated contralateral ovaries was determined. Ovaries treated with E2 averaged 3.1 +/- 0.4 oocytes while untreated ovaries in the same animals averaged 6.4 +/- 0.4 oocytes (P less than 0.001 by paired t test, n = 20). Results were similar for all amounts of E2 used and serum levels of E2 were not elevated at autopsy by this local treatment. Cholesterol alone did not alter the number of oocytes. Results of similar experiments with progesterone and dihydrotesterone were less conclusive than for E2. In additional trials, ovaries were treated with E2 as above, and preovulatory follicles were explanted on the morning of proestrus to determine their steroidogenic capability in vitro. Follicles from treated ovaries released somewhat less E2 and progesterone into luteinizing hormone (LH)-free medium than follicles from untreated ovaries, but not when LH was added to the medium.(ABSTRACT TRUNCATED AT 250 WORDS)