Differences in luteinizing hormone release stimulated in rat anterior pituitary cells by leukotriene C4 and by gonadotropin-releasing hormone in vitro

Summary Continuous administration of leukotriene C₄ (LTC₄, 10^–10 M) to superfused rat anterior pituitary cells increased LH release for 40 min only, whereas in a parallel experiment gonadotropin-releasing hormone (GnRH, 10^–9 M) evoked a continuous increase in hormone secretion. In contrast to GnRH, LTC₄ did not desensitize rat anterior pituitary cells. The secretory action resulting from the administration of LTC₄ (10^–10 M) was abolished for 40 min after previous stimulation. The results documented the dual action of LTC₄ on LH exocytosis.     

Gonadotrophin-releasing activity of histones H2A and H2B

We report that histones H2A and H2B possess gonadotrophin-releasing activity in vitro and assess the signal transduction pathways involved in these effects. Perifused and incubated rat anterior pituitary (AP) cells were used, and luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured by RIA. Perifusion of cells with histone H2A (30 μM) or histone H2B (30 μM), markedly stimulated LH release but failed to elicit any FSH response. Cells incubated with 6 or 30 μM histone H2A showed a dose- and time-dependent stimulatory effect on both LH and FSH release which was blocked by 1 μM peptide MB35, an 86–120 amino acid fragment of histone H2A. Incubation of pituitary cells with gonadotrophin-releasing hormone (GnRH) and histones H2A or H2B showed a stimulatory effect on LH and FSH release which was similar to the sum of the separate effects. Trifluoperazine, as well as ethylene glycol bis(b-aminoethyl ether) N,N,N′,N′-tetraacetic acid (EGTA), alone or in the presence of the calcium ionophore A23187, significantly reduced the response of AP cells to histones. Various cyclic adenosine monophosphate (cAMP) enhancers had no effect on histone-stimulated release of gonadotrophins in incubated AP cells. Our results confirm previous evidence that histones may act as hypophysiotrophic signals. Calcium- and diacylglycerol-associated pathways, but not cAMP, appear to participate in these effects. Received 11 August 1997; received after revision 20 January 1998; accepted 26 January 1998     

Effect of in vivo pre-treatment with oestradiol and either GnRH,GnRH agonistic analog or GnRH antagonistic analog on GnRH-stimulated secretion of LH in vitro

Summary In vivo treatment with GnRH or with GnRH agonistic analog (AG), but not with GnRH antagonistic analog (ANT), depleted the LH stores of the rat pituitary gland. This depletion was potentiated by oestradiol. Oestradiol augmented the in vitro LH response of the pituitary gland to GnRH. This augmenting effect of oestradiol became smaller with increasing rates of in vivo administration of GnRH or AG, but not with ANT. With respect to both depletion of the LH stores and suppression of the augmenting effect of oestradiol, AG ist about 20 times as potent as GnRH.     

Effect of in vivo pre-treatment with oestradiol and either GnRH, GnRH agonistic analog or GnRH antagonistic analog on GnRH-stimulated secretion of LH in vitro

In vivo treatment with GnRH or with GnRH agonistic analog (AG), but not with GnRH antagonistic analog (ANT), depleted the LH stores of the rat pituitary gland. This depletion was potentiated by oestradiol. Oestradiol augmented the in vitro LH response of the pituitary gland to GnRH. This augmenting effect of oestradiol became smaller with increasing rates of in vivo administration of GnRH or AG, but not with ANT. With respect to both depletion of the LH stores and suppression of the augmenting effect of oestradiol, AG ist about 20 times as potent as GnRH.     

Inhibition of TSH-stimulated thyroid hormone release and potentiation of TRH-stimulated TSH release by indomethacin in perifusion systems of rat thyroids and pituitaries

Using indomethacin (Ind), a prostaglandin synthesis inhibitor, in vivo experiments in rats and in vitro experiments with perifusion systems of rat thyroids and pituitaries were conducted. After 35 days of intragastric infusion of Ind, serum TSH levels were markedly increased, the thyroid was swollen and, as a consequence, T3 and T4 levels were normal. The T3 release from perifused rat thyroids under continuous stimulation with 10 mU/ml TSH was inhibited significantly (p less than 0.01) by 1.0 X 10(-6) M Ind. On the other hand, the TSH release from perifused rat pituitaries under TRH stimulation was enhanced conspicuously by Ind. It was concluded that Ind decelerated thyroid hormone release from the thyroid and accelerated TSH release from the pituitary in perifusion systems.     

Pituitary gonadotropin releasing hormone (GnRH) receptor levels in intact and ovariectomized-adrenalectomized female golden hamsters on a short photoperiod

Both intact and ovariectomized + adrenalectomized hamsters on a short photoperiod, had a daily surge in plasma LH at approximately 16.00-18.00 h. The number of pituitary GnRH receptors was generally lower in ovariectomized + adrenalectomized hamsters than in intact animals, but both intact and ovariectomized + adrenalectomized hamsters had a decrease in the number of receptors just prior to the LH surge. These results show that gonadal steroids are not involved in regulating the pre-LH surge fall in the number of GnRH receptors.     

Inhibition of prostaglandin-induced cyclic AMP accumulation in the rat anterior pituitary by alrestatin.

Alrestatin at 25-1 X 10(-4) M inhibited the accumulation of cyclic AMP induced by prostaglandin E2, but not theophylline, in the rat anterior pituitary in vitro. Somatostatin, at lower concentrations, inhibited both; maximal inhibition of the prostaglandin effect was greater with alrestatin. As cyclic AMP is considered to be a mediator in induced-hormonal release, it appears from the present findings that alrestatin may be of potential use in altering hormonal release.     

Plurihormonality in the secretory granules of the normal human pituitary. An immunoelectron microscopic study

Normal human autopsy anterior pituitary tissue from 5 cases was embedded in LR White resin and immunolabelled using silver-enhanced 5-nm protein A gold probes. Follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), adrenocorticotrophic hormone (ACTH), growth hormone (GH) and prolactin (PRL) were immunolocalised to the level of secretory granule. A two-sided double-labelling method was used to cross-react two hormones at a time with respect to their corresponding antibodies. All possible combinations of the six pituitary hormones were tested. Plurihormonal granules were found that contained LH + FSH, LH + TSH, and FSH + TSH. Each hormone was also found in monohormonal granules. Granule diameter was significantly larger in the pluri as opposed to monohormonal granules.     

Plurihormonality in the secretory granules of the normal human pituitary. An immunoelectron microscopic study

Summary Normal human autopsy anterior pituitary tissue from 5 cases was embedded in LR White resin and immunolabelled using silver-enhanced 5-nm protein A gold probes. Follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), adrenocorticotrophic hormone (ACTH), growth hormone (GH) and prolactin (PRL) were immunolocalised to the level of secretory granule.A two-sided double-labelling method was used to cross-react two hormones at a time with respect to their corresponding antibodies. All possible combinations of the six pituitary hormones were tested. Plurihormonal granules were found that contained LH+FSH, LH+TSH, and FSH+TSH. Each hormone was also found in monohormonal granules. Granule diameter was significantly larger in the pluri as opposed to monohormonal granules.     

Pituitary gonadotropin releasing hormone (GnRH) receptor levels in intact and ovariectomized-adrenalectomized female golden hamsters on a short photoperiod

Summary Both intact and ovariectomized+adrenalectomized hamsters on a short photoperiod, had a daily surge in plasma LH at approximately 16.00–18.00 h. The number of pituitary GnRH receptors was generally lower in ovariectomized+adrenalectomized hamsters than in intact animals, but both intact and ovariectomized+adrenalectomized hamsters had a decrease in the number of receptors just prior to the LH surge. These results show that gonadal steroids are not involved in regulating the pre-LH surge fall in the number of GnRH receptors.     

Inhibition of TSH-stimulated thyroid hormone release and potentiation of TRH-stimulated TSH release by indomethacin in perifusion systems of rat thyroids and pituitaries

Summary Using indomethacin (Ind), a prostaglandin, synthesis inhibitor, in vivo experiments in rats and in vitro experiments with perifusion systems of rat thyroids and pituitaries were conducted. After 35 days of intragastric infusion of Ind, serum TSH levels were markedly increased, the thyroid was swollen and, as a consequence, T₃ and T₄ levels were normal. The T₃ release from perifused rat thyroids under continuous stimulation with 10 mU/ml TSH was inhibited significantly (p<0.01) by 1.0×10^–6 M Ind. On the other hand, the TSH release from perifused rat pituitaries under TRH stimulation was enhanced conspicuously by Ind. It was concluded that Ind decelerated thyroid hormone release from the thyroid and accelerated TSH release from the pituitary in perifusion systems.     

Effects of thyroidectomy and thyroxine replacement on the responsiveness of the anterior pituitaries from male rats to thyrotropin-releasing hormone in vitro

Summary Thyroidectomy decreased prolactin concentrations in the anterior pituitary (AP) and serum of the male rat. The amount of basal and thyrotropin-releasing hormone (TRH)-stimulated release of prolactin by AP in vitro was lower in thyroidectomized (Tx) rats than in sham Tx rats. These results suggest that the inhibitory effects of thyroidectomy on pituitary and serum prolactin in male rats are mediated in part by the reduction of the production and spontaneous release of prolactin and the responsiveness of prolactin to TRH.     

The effects of vitamin E-deficiency on serum prolactin and serum luteinising hormone levels in the pregnant rat

Summary No significant differences were observed between the serum prolactin or serum LH levels of vitamin E-deficient or vitamin E-replete rats during the first 12 days of gestation. It is suggested that pituitary dysfunction is not the cause of the characteristic foetal resorption observed in vitamin E-deficient rats.Acknowledgments. The authors would like to thank Dr A.F. Parlow of the NIAMDD Rat Pituitary Hormone Distribution Programme for the generous supply of kits for the measurement of rat prolactin and LH, and Dr K.M.L. Morris (City of London Polytechnic) for arranging facilities for the radioiodination of the purified hormones used in the radioimmunoassays.     

Inhibition of LH-RH induced release of gonadotropins by substance P in cultured rat anterior pituitary cells]

Using anterior pituitary cells cultured for 7 days and then incubated for 4 hrs, substance P, an undecapeptide, inhibited the stimulatory effect of LH-RH on the release of LH-RH on the release of LH and FSH. This inhibitory effect, which was similar for both gonadotropins was only observed when the adenopituitary cells were put in culture at DI and Proestrus stages of the oestrous cycle. Furthermore substance P partly inhibited the basal release of FSH at DI and DII stages but did never affected that of LH.     

Effects of monosodium glutamate on circulating concentrations of luteinizing hormone and growth hormone in young growing domestic fowl (Gallus domesticus)

Summary The administration of monosodium glutamate (MSG) at a dose of 4 g/kg in 5-day-old fowl or 5 daily injections of MSG (total dose 20 g/kg) in 1- to 5-day-old fowl did not affect body growth in either male or female domestic fowl. Neither MSG treatment schedule affected either testis weight or the circulating concentration of luteinizing hormone (LH). A small, but significant decrease in the plasma concentration of growth hormone (GH) was observed in female chicks which had received daily MSG injections.Acknowledgments. Paper of Journal Series, New Jersey State Experiment Station, project No. 18141 and 18443, supported by State and Hatch Act funds and grants from the National Science Foundation (PCM 80227227) and the Upjohn Company.     

Influence of dopamine infusion on plasma prolactin released by kidney capsule transplanted anterior pituitaries

Summary The infusion of dopamine into the renal artery resulted in decreased prolactin release from 3 anterior pituitary glands transplanted under the kidney capsule. Prolactin levels continually decreased over a 5 min period after DA infusion was terminated and thereafter approached preinfusion levels by the end of 10 min.Supported by NSF Research, grant No. 74-17332.The authors wish to express their appreciation to Mrs Cynthia Van De Walle for her outstanding technical assistance in the performance of the prolactin RIA and the statistical analyses. We also appreciate receiving as a gift from the National Institute for Arthritis, Metabolism and Digestive Diseases the rat prolactin used for iodination (RP-I₂) and standards (RP-1).     

Hypothalamo-hypophyseal-gonadal function in the rat following administration of the novel and selective D-1 agonist CY 208-243

The effects of the novel and selective dopamine D-1 agonist CY 208-243 on the rat hypothalamo-hypophyseal-gonadal (HHG) axis were studied. CY 208-243 did not modify the concentration of luteinizing hormone (LH) in serum from female or male rats, and had no effect upon opiate antagonist-induced stimulation of LH secretion in male rats. CY 208-243 did not inhibit ovulation in cycling female rats. Thus, D-1 receptor activation by systemic drug administration does not alter HHG function in rats.     

Studies on the modulation of the desensitization of the pituitary gland by luteinizing hormone-releasing hormone in the ovariectomized rat

In ovariectomized rats the desensitization of the LH cells in vivo, which develops during constant rate infusion of LHRH, 1) does not depend on a concomitant depletion of the pituitary LH stores, 2) proceeds normally when the hypothalamo-pituitary connection has been severed and 3) is a process in which LH itself is not involved.     

Adaptation of the pituitary gland to prolonged LRH stimulation

Summary With prolonged constant rate infusion of luteinizing hormone-releasing hormone (LRH), the LH secretion rate of the rat pituitary gland changes continuously until a steady state of relative desensitization has developed. Recovery from this state can occur independently from changes in the pituitary's LH content.     

Studies on the modulation of the desensitization of the pituitary gland by luteinizing hormone-releasing hormone in the ovariectomized rat

Summary In ovariectomized rats the desensitization of the LH cells in vivo, which develops during constant rate infusion of LHRH, 1) does not depend on a concomitant depletion of the pituitary LH stores, 2) proceeds normally when the hypothalamo-pituitary connection has been severed and 3) is a process in which LH itself is not involved.