Pituitary cyclic AMP production and mechanism of luteinizing hormone release

Naor, Zvi; Koch, Yitzhak; Chobsieng, P.; Zor, U.

doi:10.1016/0014-5793(75)80288-2

Cited by 78 publications

(19 citation statements)

References 18 publications

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“…No effect of CT on basal LH release was noted in previ ous work in spite of an enhanced cAMP content [8,10,12], The data presented here may help to explain these negative findings in that the duration of the incubation in these prior studies ranged from 30 min to 4 h. Furthermore, the many experiments that attempted to mimic enhanced cell concen trations of cAMP by adding cAMP derivatives must now be reevaluated due to the provocative findings of Smith et al [11]. They demonstrated that cAMP analogues (e.g., 8-BrcAMP, dibutryl-cAMP) affected binding of GnRH to the GnRH receptor and that the effect of exogenous cAMP(i.e., 8-Br-cAMP) on LH release occurred within a few minutes, similar to the GnRH response [11].…”

Section: Discussionmentioning

confidence: 99%

Luteinizing Hormone Secretion Is Enhanced by Pertussis Toxin, Cholera Toxin, and Forskolin

Cronin¹,

Evans²,

Hewlett³

et al. 1983

Neuroendocrinology

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Pertussis toxin, cholera toxin and forskolin, all of which can increase adenylate cyclase activity, stimulated luteinizing hormone LH release from cultured rat anterior pituitary cells. Although cellular cyclic AMP and growth hormone were increased rapidly by cholera toxin and forskolin, enhanced LH release occurred significantly later with no change in total radioimmunoassayable LH (i.e., released plus stored). These data suggest that changes in cyclic AMP levels may regulate the tonic availability of releasable LH in the gonadotroph.

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Section: Discussionmentioning

confidence: 99%

Luteinizing Hormone Secretion Is Enhanced by Pertussis Toxin, Cholera Toxin, and Forskolin

Cronin¹,

Evans²,

Hewlett³

et al. 1983

Neuroendocrinology

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“…With the present experiments we aimed to in¬ vestigate a possible role for cyclic AMP in the FSH release mechanism. For this purpose hemi-pituitary glands from intact female rats were incubated with derivatives of cyclic AMP (BrcAMP, dbcAMP) and other agents which increase cyclic AMP levels in the pituitary glands (Jutisz et al 1972 ;Naor et al 1975). Obviously, the effect of these agents on FSH release may be complex, depending on the possible involvement of cyclic AMP in the stimulatory effect of LRH on FSH release and/or in the inhibitory effect of inhibin.…”

Section: Discussionmentioning

confidence: 99%

“…The effects were investigated of theophylline and the more potent phosphodiesterase inhibitor MIX as well as of NaF which stimulates cyclic AMP formation in the pituitary gland (Naor et al 1975;Jutisz et al 1972). During three separate experi¬ ments pituitary glands were incubated for 8 h in medium with 0, 1 or 10 mM of either theophylline, or MIX or NaF.…”

Section: Methodsmentioning

confidence: 99%

Divergent effects on LH and FSH synthesis and release from intact female rat pituitary glands in vitro by methylxanthines, cyclic AMP derivatives and sodium fluoride

Jenner¹,

Koning²,

Tijssen³

et al. 1985

Acta Endocrinologica

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FSH release from the female rat pituitary gland consists of an LH-like, LRH-dependent component and an autonomous, inhibin-sensitive component. It was investigated whether cyclic AMP mediated FSH release. BrcAMP, theophylline, MIX or NaF stimulated LH release but inhibited FSH release and synthesis. Although dbcAMP had no inhibitory effect on FSH release, it partly reversed the inhibitory action of theophylline. In view of previous and the present results it is concluded that cyclic AMP may mediate the LRHdependent LH and FSH release and, through a separate pathway, may mediate the inhibition of autonomous FSH release by the ovarian protein inhibin. Luteinizing hormone-releasing hormone (LRH) stimulates the release of the gonadotrophic hor¬ mones, luteinizing hormone (LH) and folliclestimulating hormone (FSH) from pituitary glands (Matsuo et al. 1971; Schally et al. 1971). Many reports deal with a possible role for cyclic AMP as an intracellular mediator for LRH-induced LH release, but only few of them also include FSH release (for review see Tixier-Vidal & Gourdji 1981; De Koning et al. 1981). Furthermore, secre¬ tion of FSH apparently is more complex than that of LH: FSH release consists of an autonomous (spontaneous or basal) component which can be inhibited by ovarian proteins (inhibin) and an LHlike, LRH-dependent component which is not af¬ fected by inhibin (Jenner et al. 1983). The present study was designed to investigate whether cyclic AMP mediates FSH release. For this purpose pitui¬ tary glands were incubated in the presence of agents that increase cyclic AMP levels. Materials and MethodsAdult female Wistar rats were decapitated on the second day of dioestrus. Two pituitary halves were placed in flasks each containing 1 ml medium TC 199 (Difco Labs.). The pre-incubation of 0.5 h and the successive 8 h incubation with fresh media were carried out at 37°C under continuous shaking and gassing with 02 and C02 (95%:5%). The following agents were dissolved in the media at final concentrations of 1 to 10 mM: 8-bromoadenosine-3':5'-mono-phosphoric acid (BrcAMP; Boeh¬ ringer), N6 -2' -0 -dibutyryl -adenosine -3',5'-monophos¬ phate (dbcAMP; Boehringer), l-methyl-3-isobutyl-xanthine (MIX; Sigma), NaF (Merck) and theophylline (DBH Chemicals Ltd.). The LH and FSH contents of the media and of saline-extracted pituitary glands were esti¬ mated by radioimmunoassay (Welschen et al. 1975;De Koning et al. 1982;Jenner et al. 1982). Since in one case (10 mM NaF treatment) pituitary wet weight was signifi¬ cantly higher, the results are expressed as µg LH-RP-1 or pg FSH-RP-1/pituitary tissue (mean ± SEM; = 4) instead of per mg pituitary wet weight (see e.g. De Koningetal. 1981Jenner et al. 1982Jenner et al. , 1983. The reference and iodination preparations were generous Table 1. ). Statistical comparisons were made by analysis of variance followed by Duncan's mul¬ tiple comparison test (Steel 8c Torrie 1960). Results Experiment 1The effects of 0, 1 and 10 mM dbcAMP in the presence and absence of 10 mM theophylline were stu...

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“…In 1975, Naor el al. [31] showed that it was possible to distinguish between the effects of LHRH on cAMPand on LH release, indicating a lack of a mechanistic relationship between these actions. Subsequent work from the laboratories of McCann [29,32], Marshall [9] and Can [10], among others, has supported this observation confirm ing an elevation of cAMP levels by LHRH, but no func tional relationship of this response to the elicitation of LH release.…”

Section: Discussionmentioning

confidence: 99%

Apparent Lack of Involvement of cAMP as a Mediator of LHRH Stimulation of Nuclear Estrogen Receptor Activity in the Rat Anterior Pituitary

Singh¹,

Bhalla²,

Muldoon³

1985

Neuroendocrinology

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We have previously shown that incubation of rat pituitary cells in the presence of LHRH results in specific enhancement of nuclear estrogen receptor (ER) binding which cannot be accounted for by simple intracellular translocation of cytoplasmic receptor. In the present study, the role of cAMP in this response has been examined. Suspended pituitary cells from adult ovariectomized rats primed with estradiol were incubated with varying concentrations of LHRH or a highly active LHRH analog (LHRH-A) for 30 min at 37 °C, and levels of cAMP were determined. Total cAMP levels changed only in response to a concentration of 100 pmol/pituitary of either peptide; the stimulation by LHRH was twice that by LHRH-A. When the priming dose level of estradiol was reduced from 1.0 to 0.5 µg/day, stimulation of cells by 100 pmol of LHRH caused a much greater increase in cAMP levels. Separate incubation of subcellular fractions with a wide dose range of dibutyryl-cAMP (DBcAMP) resulted in a progressive loss of cytosol receptor binding capacity (which was also observed in whole cultured or suspended cells), but no significant concomitant change in nuclear receptor binding; however, whole cells in suspension or culture did show an increase in nuclear ER activity in the presence of 100 nM DBcAMP. This response was qualitatively, but not quantitatively, similar to that elicited by LHRH. When the effects of whole cell incubation with LHRH and LHRH-A on nuclear ER were compared with their effects on total cAMP levels, no correlation was observed; rising levels of cAMP did, however, coincide with falling levels of cytosol ER. Integration of these observations with our previous quantitative assessment of LHRH effects on the ER populations indicates that cAMP may mediate the diminution of cytosol ER levels, but it does not appear to be involved to any appreciable degree in the enhancement of the nuclear ER binding.

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Pituitary cyclic AMP production and mechanism of luteinizing hormone release

Cited by 78 publications

References 18 publications

Luteinizing Hormone Secretion Is Enhanced by Pertussis Toxin, Cholera Toxin, and Forskolin

Luteinizing Hormone Secretion Is Enhanced by Pertussis Toxin, Cholera Toxin, and Forskolin

Divergent effects on LH and FSH synthesis and release from intact female rat pituitary glands in vitro by methylxanthines, cyclic AMP derivatives and sodium fluoride

Apparent Lack of Involvement of cAMP as a Mediator of LHRH Stimulation of Nuclear Estrogen Receptor Activity in the Rat Anterior Pituitary

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