Plasma gonadotrophin concentrations, pituitary gonadotrophin content and pituitary responsiveness to LHRH in rats treated with LHRH and oestradiol benzoate

Schuiling, G. A.; Pols-Valkhof, N.; Moes, Hendrik; Koiter, T. R.

doi:10.1677/joe.0.1150469

Cited by 9 publications

(7 citation statements)

References 17 publications

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“…Nevertheless, administration of EB on dioestrus to intact cyclic rats, a treatment that increases E 2 serum concentrations in the morning of pro-oestrus without ovarian stimulatory activity, did not reduce serum LH concentrations in pro-oestrous afternoon. By contrast, physiological doses (Schuiling et al 1987) of injected EB acted in a very convincing positive feedback manner (Fink 1988) resulting in an increased magnitude of the LH surge. Also, the observed inhibitory effect of hFSH on in vitro LH secretion from incubated pituitaries was absent in pituitaries from OVX rats.…”

Section: Discussionmentioning

confidence: 99%

“…Oestradiol benzoate (EB; Sigma Chemical Co.) was injected s.c. at the physiological doses of 10 mg/0 . 2 ml oil (Schuiling et al 1987) at 0900 h on day 3. Control rats were given 0 .…”

Section: Drugs and Treatmentsmentioning

confidence: 99%

“…Besides this steroidogenic activity, a significant number of FSH-dependent non-steroidal substances of ovarian origin with regulating activities on the synthesis and release of gonadotrophins (LH and FSH) have recently been identified. Inhibin, activin and follistatin are relatively stronger modulators of FSH secretion (Farnworth et al 1988, de Jong 1988, Ying 1988, whereas gonadotrophin surge-inhibiting or -attenuating factor (GnSI/AF, also named attenuin; Balen 1996, Fowler et al 2003 and oestrogen-antagonizing factor (Schuiling et al 1987(Schuiling et al ,1999 are relatively stronger suppressors of the preovulatory LH surge.…”

Section: Introductionmentioning

confidence: 99%

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The ovary-mediated FSH attenuation of the LH surge in the rat involves a decreased gonadotroph progesterone receptor (PR) action but not PR expression

Gordon

Garrido‐Gracia

Aguilar

et al. 2007

Journal of Endocrinology

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Hyperstimulation of ovarian function with human FSH (hFSH) attenuates the preovulatory surge of LH. These experiments aimed at investigating the mechanism of ovarian-mediated FSH suppression of the progesterone (P 4 ) receptor (PR)-dependent LH surge in the rat. Four-day cycling rats were injected with hFSH, oestradiol benzoate (EB) or vehicle during the dioestrous phase. On pro-oestrus, their pituitaries were studied for PR mRNA and protein expression. Additionally, pro-oestrous pituitaries were incubated in the presence of oestradiol-17b (E 2 ), and primed with P 4 and LH-releasing hormone (LHRH), with or without the antiprogestin RU486. After 1 h of incubation, pituitaries were either challenged or not challenged with LHRH. Measured basal and LHRH-stimulated LH secretions and LHRH self-priming were compared with those exhibited by incubated pituitaries on day 4 from ovariectomized (OVX) rats in metoestrus (day 2) injected with hFSH and/or EB on days 2 and 3. The results showed that: i) hFSH lowered the spontaneous LH surge without affecting basal LH and E 2 levels, gonadotroph PR-A/PR-B mRNA ratio or immunohistochemical protein expression; ii) incubated pro-oestrous pituitaries from hFSH-treated rats did not respond to P 4 or LHRH, and lacked E 2 -augmenting and LHRH self-priming effects and iii) OVX reversed the inhibitory effects of hFSH on LH secretion. It is concluded that under the influence of hFSH, the ovaries produce a non-steroidal factor which suppresses all PR-dependent events of the LH surge elicited by E 2 . The action of such a factor seemed to be due to a blockade of gonadotroph PR action rather than to an inhibition of PR expression.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Oestradiol benzoate (EB; Sigma Chemical Co.) was injected s.c. at the physiological doses of 10 mg/0 . 2 ml oil (Schuiling et al 1987) at 0900 h on day 3. Control rats were given 0 .…”

Section: Drugs and Treatmentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The ovary-mediated FSH attenuation of the LH surge in the rat involves a decreased gonadotroph progesterone receptor (PR) action but not PR expression

Gordon

Garrido‐Gracia

Aguilar

et al. 2007

Journal of Endocrinology

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“…Thus, it has been shown that oxytocin is intimately involved in the control of LH release. However the LH releasing activity of oxytocin is demonstrable only at proestrus and not on the other days of the cycle.A similar cycle dependency, with heightened respon siveness on proestrus, is demonstrable for GnRH activ ity [3][4][5], In part this results from an interplay of the varying estradiol and progesterone levels during the es trous cycle, which exert both positive and negative ef Received: November 26, 1990 Accepted after revision: September 18. 1991 fects on the hypothalamohypophyseal system [6,7].…”

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confidence: 85%

Luteinizing Hormone Response to Oxytocin Is Steroid-Dependent

Evans

Robinson²,

Catt³

1992

Neuroendocrinology

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Oxytocin-induced LH release from dispersed rat anterior pituitary cells in vitro was shown to be dependent on the steroidal environment. Preincubation of anterior pituitary cells with estradiol for 48 h enhanced the subsequent LH response to oxytocin (p < 0.001). Maximal sensitization was observed with estradiol at 1 nM. Release of LH induced by oxytocin was inhibited in the presence of progesterone or to a greater extent in the presence of equimolar testosterone. Complete suppression of oxytocin-induced LH secretion occurred with 1 nM progesterone. Incubation of hemipituitaries with oxytocin revealed that the pituitary was sensitive in vitro to oxytocin at proestrus (p < 0.05) but not at other stages of the cycle. The results indicate that there is altered sensitivity to oxytocin of the pituitary at different stages of the estrous cycle. Therefore activity of the neuropeptide in vivo might be modulated by steroids.

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“…The ef¬ fect of E2 remains suppressive (Schuiling et al ,1987. Only after termination of GnRH treat¬ ment does the augmenting effect of E, appear again (Schuiling et al 1985).…”

mentioning

confidence: 99%

Effect of estradiol on the secretion of LH in the GnRH-pretreated rat after treatment with the GnRH-antagonist, Org 30093

Schuiling

Valkhof²,

Koiter³

1988

Acta Endocrinologica

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LH responses induced in the long-term ovariectomized rat by GnRH or GnRH agonistic analogue are augmented by E2. The augmentation by E2 does not occur during, but after termination of GnRH pretreatment. In this study it was investigated whether the augmenting effect of E develops also in the GnRH-pretreated rat when the animals were treated with GnRH antagonistic analogue. Two weeks after ovariectomy rats were treated for 10 days with 250 ng GnRH/h (GnRH\x=req-\ rats), released by sc implanted osmotic minipumps. Control rats received a Silastic 'sham pump'. Rats were simultaneously treated with solvent (oil) or estradiol benzoate (EB, 3 \ g=m\ g,sc). Each group of rats was divided into two subgroups, one receiving solvent, the other the GnRH antagonist, Org 30093 (ANT, 100 \g=m\g/injection) on 3 consecutive days. In Experiment 1, the pituitary LH content and the LH secretion following stimulation with the agonistic GnRH analogue buserelin, were measured, in Experiment 2, the plasma concentrations of LH before and after cessation of ANT treatment. The effects of treatment with GnRH, EB and ANT were studied on the basis of 1) the height of the maximal LH response and 2) the halfmaximally effective dose (ed 50) of buserelin. Experiment 1 revealed that GnRH depleted the pitutiary gland to about 42% of its original LH content. In EB-treated GnRH-rats the depletion was even stronger (to 14%). After ANT treatment, the pituitary glands of the GnRH\x=req-\ rats were (partly) repleted (oil: to 65%; EB: to 31%). ANT and EB had no effect on the pituitary LH content in control rats. EB increased the maximal LH response in control rats but not in GnRH-rats. ANT increased the maximal LH response to buserelin in oil-injected control rats as well as in oil-and EB-treated GnRH-rats. In these latter two groups, the increase of the maximal LH response was equally large. However, there was an effect of EB on the ed 50 of buserelin during ANT treatment, the pituitary gland of the EB-treated GnRH-rats had become more sensitive to GnRH. Experiment 2 revealed that GnRH pretreatment reduced the plasma LH concentrations to about 49% of the control levels. EB and ANT, too, lowered the plasma LH concentrations (to about 25%). Neither EB nor ANT, alone or in combination, changed the plasma LH concentrations in GnRH-rats. After cessation of ANT treatment, the plasma LH levels of the oil-injected control rats slowly returned to pretreatment levels, but those of the EB-treated control rats remained suppressed. In the GnRH-rats the reverse was seen: after cessation of ANT treatment, peaks of LH appeared in the plasma of the EB-treated rats, but not in the oil-injected. It is concluded that 1) treatment with ANT is not fully equivalent to termination of GnRH administration because it antagonizes the effects of GnRH only in part: 2) ANT has an intrinsic augmenting effect on the pituitary GnRH-responsiveness, and 3) owing to E2-induced sensitization of the pituitary gland, peaks of LH appear in the plasma of GnRH-rats but not of control rats after t...

show abstract

Plasma gonadotrophin concentrations, pituitary gonadotrophin content and pituitary responsiveness to LHRH in rats treated with LHRH and oestradiol benzoate

Cited by 9 publications

References 17 publications

The ovary-mediated FSH attenuation of the LH surge in the rat involves a decreased gonadotroph progesterone receptor (PR) action but not PR expression

The ovary-mediated FSH attenuation of the LH surge in the rat involves a decreased gonadotroph progesterone receptor (PR) action but not PR expression

Luteinizing Hormone Response to Oxytocin Is Steroid-Dependent

Effect of estradiol on the secretion of LH in the GnRH-pretreated rat after treatment with the GnRH-antagonist, Org 30093

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