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

Braw, Ruth H.; Tsafriri, A.

doi:10.1530/jrf.0.0590259

Cited by 73 publications

(41 citation statements)

References 15 publications

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“…The amount of androstenedione used (0-1-1 0 µ ) might have saturated the system so that oestradiol synthesis plateaued. The fact that the 2-day delayed follicles were able to produce oestradiol in vitro at a level similar to controls (Table 1) contrasts with previous models using barbiturates (Uilenbroek, Woutersen & van der Schoot, 1980 ;Braw & Tsafriri, 1980;Terranova, 1981) in which oestradiol secretion by 2-day delayed follicles was reduced. The exogenous LH may maintain oestradiol secretion by the follicles through enhancement of aromatase ; however, the number of granulosa cells may be greater than in controls since the LH-treated follicles are larger.…”

Section: Resultscontrasting

confidence: 73%

Elevated peripheral concentrations of LH block ovulation and increase thecal and serum progesterone in the hamster

Rousey¹,

Terranova²

1985

Reproduction

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Summary. Insertion of osmotic minipumps containing 1 mg ovine LH on Day 1 (oestrus) elevated circulating serum concentrations of LH, progesterone and androstenedione when compared with values at pro-oestrus. Ovulation was blocked for at least 2 days at which time there were twice the normal numbers of preovulatory follicles. Follicular and thecal progesterone production in vitro was elevated when compared with that in pro-oestrous controls. Follicular and thecal androstenedione production in vitro was lower than in controls even though serum concentrations of androstenedione were elevated; the higher androstenedione values may be due to the increase in number of preovulatory follicles when compared with pro-oestrous controls.Follicles from LH-treated hamsters aromatized androstenedione to oestradiol and follicular production of oestradiol was similar to that in pro-oestrous follicles despite low follicular androstenedione production in the LH-treated group. Treatment with 20 i.u. hCG on Days 4 or 6 after insertion of an LH osmotic minipump on Day 1 induced ovulation of~30 ova, indicating that the blockade of ovulation was not due to atresia of the preovulatory follicles. Serum progesterone concentrations on Days 2, 4 and 6 in LH-treated hamsters were > 17 nmol/l, suggesting that the blockade of ovulation might have been due to prevention of the LH surge by high serum progesterone concentrations.

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Section: Resultscontrasting

confidence: 73%

Elevated peripheral concentrations of LH block ovulation and increase thecal and serum progesterone in the hamster

Rousey¹,

Terranova²

1985

Reproduction

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“…Inhibition of the LH surge by hypophysectomy or pentobarbital treatment causes the follicles to degenerate (Talbert et al, 1951;Braw and Tsafriri, 1980). The decrease in spontaneous apoptosis observed in isolated preovulatory rat follicles treated with hCG to stimulate the LH receptor may be mediated, at least in part, by endogenous production of pituitary adenylate cyclase-activating polypeptide (PACAP).…”

Section: Periovulatory Folliclesmentioning

confidence: 99%

Survival factors regulating ovarian apoptosis -- dependence on follicle differentiation

Markström¹,

Svensson²,

Shao³

et al. 2002

Reproduction

203

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Only a minute fraction of the ovarian follicles present in a fetal ovary will complete the path to ovulation. Most of the follicles will undergo atresia, a hormonally controlled apoptotic process. Apoptosis occurs at each stage of follicular development and there is a marked reduction in the number of follicles present at birth. Stage-dependent mechanisms of follicle survival can be postulated to achieve co-ordinated development, leading to ovulation of a small fraction of follicles. Indeed, hormone and growth factor regulation of follicular atresia is stage-specific. This short review considers the factors that promote survival of ovarian follicles throughout development, including endocrine, locally produced and intracellular mediators, as exemplified mainly by follicular development in rodents. In primordial follicles, oocyte apoptosis is considered to be the cause of subsequent follicle degeneration. In slow-growing preantral follicles, FSH is not a survival factor, but some locally produced growth factors are. Progression to the antral follicle stage is probably the most critical stage of follicle development in vivo, and FSH is a major survival factor at this stage. In addition, insulin-like growth factor I and interleukin 1beta are potent survival factors for cultured rat follicles at the antral stage. Preovulatory follicles express receptors for LH, and both of the gonadotrophins are survival factors at this stage. Relatively little is known about the period between the LH surge and ovulation; however, it has been suggested that at this stage progesterone acts as a survival factor.

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“…It has been shown that atresia is associated with an increase in follicular progesterone production (McNatty, 1980;Braw & Tsafriri, 1980;Terranova, 1981 …”

Section: Inhibinmentioning

confidence: 99%

Oocyte maturation inhibitor, inhibin and steroid concentrations in porcine follicular fluid at various stages of the oestrous cycle

Wiel¹,

Bar‐Ami²,

Tsafriri³

et al. 1983

Reproduction

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

Abstract: Summary. Graafian follicles from rats treated for 1 or 2 days with pentobarbitone sodium (Nembutal)

Cited by 73 publications

References 15 publications

Elevated peripheral concentrations of LH block ovulation and increase thecal and serum progesterone in the hamster

Elevated peripheral concentrations of LH block ovulation and increase thecal and serum progesterone in the hamster

Survival factors regulating ovarian apoptosis -- dependence on follicle differentiation

Oocyte maturation inhibitor, inhibin and steroid concentrations in porcine follicular fluid at various stages of the oestrous cycle

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