The self-priming action of LHRH increases the low pituitary LH and FSH response caused by ovarian factors: observations in vitro

Koning, J. de; Tijssen, A. M. I.; Rees, G. P. van

doi:10.1677/joe.0.1200439

Cited by 19 publications

(16 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, those investigators who observed that FF interfered with the primary LH rise also reported that FF blunted GnRH-induced LH secretion (9). Pituitary responsiveness to GnRH is maximum during proestrus (25), a phenomenon which may, at least in part, reflect the self-priming effect of GnRH on LH release (26)(27)(28). Ovarian factors distinct from inhibin attenuate this self-priming effect (29)(30)(31), but to our knowledge the ability of rh inhibin to achieve a similar effect has not been investigated.…”

Section: Discussionmentioning

confidence: 99%

Effect of Recombinant Inhibin on Gonadotropin Secretion during Proestrus and Estrus in the Rat*

Rivier

Schwall²,

Mason³

et al. 1991

Endocrinology

View full text Add to dashboard Cite

This work investigated the ability of recombinant human (rh) inhibin A or the GnRH antagonist [Ac-D2Nal1, delta Cpa2, delta 3Pal3, Arg5 delta 5-(p-methoxyphenyl)5-oxo-2-aminopentanoic acid6, delta Ala10]GnRH to alter plasma immunoreactive LH and FSH levels in cycling female rats. In a first series of experiments, rh inhibin A (25 micrograms/kg) was injected iv between 0800 and 0830 h, or at 0800 and 1200 h, on proestrus, and plasma hormone levels were measured from 1200-1900 h. Both regimens of administration significantly (P less than or equal to 0.01) lowered mean plasma FSH levels but did not mask the primary FSH surge. This treatment also lowered the overall amount of LH released, although the difference between control and inhibin-treated rats only reached statistical significance (P less than or equal to 0.05) after two injections of the protein. Measurement of the number of tubal ova shed on the next estrus showed no difference between rats injected with the vehicle or inhibin at 0830 h. Finally, it was shown that administration of the GnRH antagonist (100 micrograms/kg) at 1200 h interfered with the primary surges of both LH and FSH. In a second series of experiments, rh inhibin A (25 micrograms/kg) was injected once at 2000 h on proestrus. In these animals, inhibin significantly (P less than or equal to 0.01) decreased mean plasma FSH levels between 2000 h on proestrus and 0500 h on estrus and totally suppressed the secondary FSH surge. LH secretion remained low in control animals, and no measurable changes were observed after inhibin treatment. Flushing of the ova 5 days later (i.e. during estrus of the subsequent cycle) showed no difference between control and inhibin-treated rats. Injection of the GnRH antagonist (100 micrograms/kg) at 2000 h on proestrus decreased the total amount of FSH secreted during late proestrus and early estrus. However, FSH secretion showed an increase at between 0100 and 0400 h of estrus despite blockade of GnRH receptors. These results indicate that administration of rh inhibin A interferes with both the primary and secondary FSH surges. In contrast to its inability to alter LH release by ovariectomized rats, inhibin also blunted LH secretion during the afternoon of proestrus. Whether these results represent differential effects of inhibin on LH secreted by intact and gonadectomized animals, or whether the documented changes in pituitary responsiveness to GnRH during proestrus are accompanied by an increased sensitivity to inhibin, needs further investigation.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of Recombinant Inhibin on Gonadotropin Secretion during Proestrus and Estrus in the Rat*

Rivier

Schwall²,

Mason³

et al. 1991

Endocrinology

View full text Add to dashboard Cite

show abstract

“…The ovarian protein factor was called gonadotropin surge-inhibiting factor (GnSIF) (14). Many studies have been devoted to the mechanisms involved in the self-priming action of GnRH (15)(16)(17)(18)(19)(20), but relatively few studies have addressed the question of how a suppressive feedback mechanism is established at the pituitary level. Recently, it was suggested that inter¬ cellular communication involving different pituitary cell types may well play a role in the establishment of a biphasic LH secretion response to GnRH (21).…”

mentioning

confidence: 99%

“…Previous in vitro studies on the restoration of a biphasic LH secretion response to GnRH were either performed in hemipituitaries (18) or in monolayer cultures of dispersed pituitary cells (24,25). Therefore, the focus of the present study was twofold.…”

mentioning

confidence: 99%

Influence of folliculo-stellate cells on biphasic luteinizing hormone secretion response to gonadotropin-releasing hormone in rat pituitary cell aggregates

Allaerts

Tijssen²,

Jeucken³

et al. 1994

European Journal of Endocrinology

View full text Add to dashboard Cite

Anterior pituitary cells cultured as three-dimensional cell aggregates and incubated with gonadotropin-releasing hormone (GnRH) show a biphasic pattern of luteinizing hormone (LH) release when steroid-free bovine follicle fluid is added to the culture medium. Initially, the GnRH-induced LH release is low (lag-phase response), but LH release increases during further incubations with GnRH (primed-state response). Also, in aggregates of dispersed cells from long-term ovariectomized rats cultured for 2 days in the presence of 1% bovine follicle fluid, a low initial LH responsiveness to GnRH could be restored. Cycloheximide was found to block the induction of the primed state, indicating the protein synthesis dependency of GnRH self-priming. In aggregates from gonadotroph-enriched cell populations obtained by velocity sedimentation in a bovine serum albumin gradient, addition of 1% bovine follicle fluid to the culture medium also restored a biphasic pattern of GnRH-induced LH release. However, co-culturing the gonadotroph-enriched cell aggregates with a folliculo-stellate (FS) cell-enriched population resulted in the attenuation of the differences in LH secretion rate between early and late responses to GnRH. The present example of the attenuation by folliculo-stellate cells of pituitary hormone secretion responses demonstrates that the cells regulate the cellular processes leading to a priming of the LH response to GnRH, rather than interfering with the access of GnRH to its receptor in gonadotrophs. Finally, it was found that stimulation of the adenylate cyclase enzyme with maximal effective doses of forskolin counteracted the inhibitory effect of bovine follicle fluid on the initial LH response to GnRH, but did not completely abolish the biphasic pattern of LH release. It is concluded that coupling to the adenylate cyclase enzyme is presumably involved in the LH surge inhibiting feedback action on the pituitary cells, but also other messenger pathways and intercellular interactions between pituitary cells may play a role in establishing a biphasic LH release at the pituitary level following GnRH administration.

show abstract

“…The animals were decapitated at 0900 h. In one series of experiments, the extracted hypophyses were divided into two halves, and two halves of different hypophyses each were placed after weighing into incubation flasks containing 1 ml of medium 199, saturated in an atmosphere of 95% 02 + 5% CO 2 [16]. The incubation was carried out at 37~C with constant agitation.…”

Section: Methodsmentioning

confidence: 99%

State of hypophyseogonadal system in male rats with diabetes (experimental investigation)

Babichev

Peryshkova

Adamskaya

1994

Neurosci Behav Physiol

View full text Add to dashboard Cite

It is well known that the neuroendocrine regulation of the reproductive function in male rats is disturbed in diabetes; however, so far there is more than one opinion regarding the level at which these changes take place. The published data relating to the secretion of gonadotropins are highly contradictory: a decreased [20] or unchanging [8] level of the circulating gonadotropins in the blood has been demonstrated. The majority of investigators are in agreement that a decreased level of androgens is observed in diabetic patients [9,20], which attests to a disturbance in the negative feedback mechanism. Both the hypothalamus and the hypophysis may be the locus of decreased sensitivity to androgens in such animals.In our preceding study we investigated the disturbance of negative feedback at the level of the mediobasal hypothalamus (MBH), and did not find alterations in the concentration of the nuclear receptors of androgens in this region. Since the effect of the sex steroids on the secretion of gonadotropins is mediated through specific receptors, this mechanism apparently remains undamaged at the level of the hypothalamus.In this connection, the state of the hypophyseogonadal system was investigated in the present study in male rats with experimental diabetes. For this purpose, an analysis was made of the sensitivity of the hypophysis to luliberin (LH-RH), and the concentration of the nuclear receptors of the sex hormones in the adenohypophysis that participate in the regulation of the secretion of gonadotropins through the negative feedback mechanism was determined in male rats

show abstract

The self-priming action of LHRH increases the low pituitary LH and FSH response caused by ovarian factors: observations in vitro

Cited by 19 publications

References 21 publications

Effect of Recombinant Inhibin on Gonadotropin Secretion during Proestrus and Estrus in the Rat*

Effect of Recombinant Inhibin on Gonadotropin Secretion during Proestrus and Estrus in the Rat*

Influence of folliculo-stellate cells on biphasic luteinizing hormone secretion response to gonadotropin-releasing hormone in rat pituitary cell aggregates

State of hypophyseogonadal system in male rats with diabetes (experimental investigation)

Contact Info

Product

Resources

About