bluuebunny/crossref_metadata_2025_split huggingface dataset:
Formation of releasable γ-aminobutyrate from putrescine by rat adrenal slices in vitro
Authors: Oon B. B. , Scraggs P. R. , Gillham B. 
Published: December 2008

ABSTRACT
Rat adrenal gland slices, when incubated in vitro with [1,4-14C]putrescine, accumulate the radioactive diamine and convert it, in part, to a compound indistinguishable (in four separative systems) from [14C]γ-aminobutyrate (GABA). Adrenal glands taken from animals that had undergone adrenal enucleation 28 days previously, so that the cortex of the tissue had regenerated, likewise formed [14C]GABA from [1,4-14C]putrescine. Putrescine-derived GABA was released from adrenal slices in vitro by 48 mmol K+/l, the release being dependent upon the presence of Ca2+ in the incubation medium. ACTH(1–24) and 8-bromocyclic AMP both provoked a dose-related release of putrescine-derived GABA, although the dose–response curve for the latter differed somewhat from that for the release of corticosterone by this secretogogue.
The enzyme believed to be responsible for the first step in the metabolic transformation of putrescine into GABA, diamine oxidase (DAO), is present in extracts of adrenal tissue and its catalytic activity underwent a transient increase followed by a fall below resting levels upon stimulation of adrenal slices with ACTH(1–24). The conclusion that this enzyme initiates the formation of GABA by this pathway is indicated by the observation that adrenal slices pretreated with the DAO inhibitor, aminoguanidine, released significantly less [1,4-14C]putrescine-derived GABA in response to 48 mmol K+/l than did control tissues. The functional significance of these findings remains to be established.
Journal of Endocrinology (1989) 123, 227–232
Failure of N-(2,4-dinitrophenyl)-5-methoxytryptamine (a putative melatonin antagonist) and of N-(3,5-dinitrophenyl)-5-methoxytryptamine to prevent the effects of injections of melatonin in the late afternoon on testicular activity of the golden hamster
Authors: Pévet P. , Masson-Pévet M. , Chantegrel J. , Marsura A. , Luu-Duc C. , Claustrat B. 
Published: December 2008

ABSTRACT
Daily injections of 10 μg melatonin in the late afternoon into male golden hamsters kept under a long photoperiod (14 h light: 10 h darkness) and at low ambient temperature 6 ± 1 °C) induced a complete gonadal atrophy after 4 weeks. When administered under the same conditions at doses of 25 μg, neither N-(3,5-dinitrophenyl)-5-methoxytryptamine or N-(2,4-dinitrophenyl)-5-methoxytryptamine, a putative melatonin antagonist termed ML-23 in the literature, showed any effect on testicular activity. Moreover, these two drugs were also unable to prevent melatonin-induced gonadal atrophy when injected 30 min before melatonin.
The results demonstrate that in the golden hamster and in the present experimental conditions, these drugs do not have the melatonin-antagonistic properties as described in the rat.
Journal of Endocrinology (1989) 123, 243–247
Interdependence of oestradiol and 5α-dihydrotestosterone in modulating LH and FSH secretion in rats
Authors: Schuiling G. A. , Moes H. , Koiter T. R. 
Published: December 2008

ABSTRACT
The effects of oestradiol, 5α-dihydrotestosterone (DHT) and oestradiol plus DHT on pituitary responsiveness to LHRH were studied. Rats ovariectomized for 2 weeks were infused s.c. (by osmotic minipump) with LHRH at 250 ng/h for 6 days. Control rats received a sham s.c. pump. On day 3, silicone elastomer implants containing oestradiol or DHT were implanted s.c., and on day 6 the effects of these in-vivo treatments on pituitary LH and FSH content and on in-vitro (perifusion) LH and FSH secretion following maximal LHRH stimulation (1 μg/ml perifusion medium) were assessed.
Luteinizing hormone-releasing hormone alone decreased pituitary LH/FSH content and, in response to acute LHRH challenge in vitro, the absolute rate of LH/FSH release, but not LH/FSH release expressed as a fraction of pituitary content. Oestradiol alone increased pituitary LH/FSH content and LHRH-induced LH/FSH release in vitro, both absolutely and as a fraction of pituitary LH/FSH. Oestradiol exacerbated the decrease in pituitary LH/FSH caused by LHRH pretreatment in vivo, and decreased the absolute rate of LHRH-stimulated LH/FSH release in vitro, but increased this rate when it was expressed as a fraction of pituitary LH/FSH. In both LHRH-treated and control rats, DHT increased pituitary LH/FSH content, did not change the absolute rate of LH/FSH release in response to acute LHRH challenge in vitro, but decreased the rate of LH/FSH release expressed as a fraction of pituitary LH/FSH content. Combined pretreatment with oestradiol and DHT resulted in both control and LHRH-treated rats having pituitary contents comparable with those produced by DHT, similar fractions of pituitary LH/FSH release to those produced by oestradiol, and absolute rates of LH and FSH release following LHRH stimulation that were generally greater than those of the respective controls and those following other steroid pretreatment regimens. It is suggested that depletion of pituitary gonadotrophin stores caused by LHRH pretreatment in vivo, not desensitization, is responsible for the reduced LH/FSH release to an LHRH challenge in vitro and that, in the female, because of the presence of oestrogens, androgens do not exert a negative feedback on the pituitary gland as they do in the male, but, on the contrary, contribute to a high level of pituitary LHRH responsiveness.
Journal of Endocrinology (1989) 123, 257–262
Diminished role of LHRH in the control of gonadotroph morphology and function in the long-term castrated male rat
Authors: Almeida O. F. X. , Hassan A. H. S. , Nikolarakis K. E. , Martin G. B. 
Published: December 2008

ABSTRACT
It was found in previous studies that the neurotransmitter control of the secretion of LHRH and LH differs between long-term castrated and ovariectomized rats. One interpretation of these data was that there was a reduced 'positive drive' in the male, and the question was raised 'how do the gonadotrophs of long-term castrated rats maintain a high level of LH secretion?'. In the present series of experiments, evidence for a reduced dependence of the gonadotrophs upon LHRH stimulation is provided. Although sensitivity to native LHRH was not completely lost in long-term castrated rats, two potent LHRH antagonists (d-pyroglu1,d-Phe2,d-Trp3,6)-LHRH and (N-acetyl-3,4-dehydro-Pro,p-fluoro-d-Phe2,d-Trp3,6)-LHRH, were found to inhibit LH secretion in short-term castrated and long-term ovariectomized rats, but not in long-term castrated rats. Neither blockade of axonal transport with colchicine nor immunoneutralization of LHRH with an antiserum against LHRH (both administered 48 h before blood sampling) produced reductions in serum concentrations of LH in long-term castrated rats, although these treatments significantly suppressed LH levels in short-term castrated animals. Chronic (6-day) infusions of the second LHRH antagonist (up to 450 μg/day) neither reduced LH secretion nor altered the morphology of the 'castration cells' in the pituitaries of long-term castrated rats. Chronic treatment with testosterone (15 days), however, reversed these parameters to some extent, and when the testosterone treatment was coupled with chronic infusions of the LHRH antagonist, significantly lower serum levels of LH and reductions in the size of the castration cells were observed. These data thus indicate that castration cells may function autonomously, without the need for LHRH, and that testosterone in some way restores the dependency on LHRH and/or the responsiveness to LHRH of these cells.
Journal of Endocrinology (1989) 123, 263–273
Influence of the thymus on steroidogenesis by rat ovarian cells in vitro
Authors: Aguilera G. , Romano M. C. 
Published: December 2008

ABSTRACT
Thymic hormones and factors have been shown to modulate the function of other endocrine glands including the gonads. Absence of the thymus during development results in ovarian dysgenesis characterized by a decrease in the number of follicles and corpora lutea, bringing about severe changes in reproductive function.
To examine whether thymic secretions might affect ovarian activity, whole dispersed ovarian cells obtained from immature rats pretreated with pregnant mare serum gonadotrophin were exposed to a thymus fraction of approximately 28 kDa and also to the media from incubated thymuses (TIM) and the conditioned media from cultured thymic reticuloepithelial cells (TCM).
The thymic fraction caused a dose-dependent decrease in human chorionic gonadotrophin (hCG)-stimulated production of progesterone, oestradiol and testosterone, but had no effect on their synthesis in the absence of hCG. Similarly, hCG-induced production of these steroids was decreased by TIM and TCM. Progesterone secretion was the most markedly affected.
These results suggest: (1) that the thymus contains a factor with a molecular weight of approximately 28 kDa which interacts with hCG in ovarian cells, (2) that the thymus can release active substances which modify steroid secretion by the ovary in vitro and (3) that the reticuloepithelial cells of the thymus are involved in the secretion of factors which modulate the stimulation by hCG of steroidogenesis in ovarian cells.
Journal of Endocrinology (1989) 123, 367–373
Passively immunizing ewes against inhibin during the luteal phase of the oestrous cycle raises the plasma concentration of FSH
Authors: Mann G. E. , Campbell B. K. , McNeilly A. S. , Baird D. T. 
Published: December 2008

ABSTRACT
Passive immunization was used to investigate the importance of inhibin in the negative feedback loop regulating the production of FSH in sheep. An antiserum raised to the 1–26 peptide fragment of the N-terminus of the α-chain of porcine inhibin was first shown to neutralize the suppressive effects of inhibin on the production of FSH by dispersed ovine pituitary cells in vitro. Groups of five mature Scottish Blackface ewes on day 8 of the luteal phase of the oestrous cycle were then injected with either 10 ml plasma from normal ewes (control) or 10 ml ovine inhibin antiserum. On day 10, luteal regression was induced by an i.m. injection of cloprostenol (100 μg), and ovulation rate determined 6 days later by laparoscopy. Peripheral plasma samples were collected throughout the experimental period.
Following treatment, there was no change in the peripheral plasma concentration of LH in either group. Following injection of the inhibin antiserum, the concentration of FSH rose significantly (P<0·001) compared with the control group. The concentration of FSH rose from 1·42 ± 0·06 to a maximum of 2·58 ± 0·23 (s.e.m.) μg/l by 5·6 ±0·9 h, this maximum lasting 9·0±1·1 h. By 32·8 ±6·9 h, the concentration of FSH had returned to pretreatment levels, while the titre of free antibody in the plasma of treated ewes was still high. In the treated ewes, there were one single and four double ovulations compared with three single and two double ovulations in the control group, indicating that the inhibin immunization may have resulted in an increase in ovulation rate.
We conclude that the marked rise in the plasma concentration of FSH following injection of inhibin antiserum provides strong evidence that inhibin is an important factor in the regulation of FSH production by the pituitary gland at this time.
Journal of Endocrinology (1989) 123, 383–391
Activation of pituitary-adrenal function in fetal sheep by corticotrophin-releasing factor and arginine vasopressin
Authors: Brooks A. N. , White A. 
Published: December 2008

ABSTRACT
In sheep, birth is preceded by an increase in fetal plasma concentrations of ACTH and cortisol. Activation of the fetal pituitary-adrenal axis is pivotal to the onset of parturition in this species and may be regulated, at least in part, by corticotrophin-releasing factor (CRF). Pulsed administration of CRF has been shown to activate the fetal pituitary-adrenal axis in immature fetal sheep. However, pituitary ACTH responsiveness declined after continued administration of CRF, as a result of increasing negative feedback effects of increased concentrations of endogenous cortisol. To test the hypothesis that arginine vasopressin (AVP) is required, in addition to CRF, to produce the necessary trophic stimulus to the pituitary-adrenal axis, we administered saline, CRF (1 μg), AVP (200 ng) or CRF plus AVP as pulses every 4 h for 7 days to fetal sheep beginning at days 117–120 of pregnancy (term =145 days). Pituitary-adrenal responses were assessed by measuring plasma concentrations of immunoreactive (ir) ACTH and cortisol in response to one of the pulses on each of the 7 days of treatment.
On day 1, CRF and AVP significantly increased plasma concentrations of ir-ACTH and there was a synergistic interaction when the two peptides were given together (P<0·05). However, as pulsed treatment continued there was a decline in the pituitary ir-ACTH response to all treatments (P<0·05). This decline in pituitary response occurred over a much longer period of time when CRF and AVP were given together when compared with the two peptides given separately. In contrast, the cortisol response to endogenously released ir-ACTH after administration of CRF, AVP or CRF plus AVP was small on day 1 but gradually increased as treatment progressed. This was particularly apparent when the two peptides were given together. A significant inverse correlation (r = 0·781, P<0·01) between basal cortisol concentrations and the ir-ACTH response to CRF plus AVP was observed over the 7 days of treatment. Premature delivery was not induced by any of the treatments despite significant increases in fetal adrenal weight. Furthermore, there were no changes in the circulating maternal plasma concentrations of progesterone or oestrone during the 7 days of the experiment.
We conclude that combination of CRF and AVP administered as pulses to immature fetal sheep results in a greater degree of pituitary-adrenal activation when compared with the two peptides given independently. However, even after this combined treatment regimen pituitary responsiveness eventually declines, an effect which may be due to increased negative feedback effects of increased endogenous cortisol.
Journal of Endocrinology (1990) 124, 27–35
Metabolic responses to euglycaemic hyperinsulinaemia in lactating and non-lactating sheep in vivo
Authors: Faulkner A. , Pollock H. T. 
Published: December 2008

ABSTRACT
Glucose utilization and production and changes in concentrations of plasma metabolites were studied in lactating and non-lactating sheep in response to three levels of insulin infusion whilst maintaining euglycaemia. Glucose utilization and production responded to insulin infusion similarly in both lactating and non-lactating ewes but, as circulating concentrations of insulin were lower in lactating animals, these parameters appeared more sensitive to plasma concentrations of insulin in lactating sheep. Changes in plasma concentrations of glycerol and free fatty acids during lactation indicated reduced sensitivity to insulin in adipose tissue and changes in plasma concentrations of amino acids were also less during lactation, suggesting reduced sensitivity of protein synthesis to insulin. Changes in plasma concentrations of urea and β-hydroxybutyrate during lactation were similar to those in non-lactating animals, indicating similar insulin sensitivity of hepatic metabolism. It is concluded that during lactation ovine adipose tissue and muscle are more resistant to increased concentrations of insulin but that the sensitivity of the sheep liver is unchanged or increased. The rate of removal of insulin from the circulation was higher in lactating animals.
Journal of Endocrinology (1990) 124, 59–66
A central action of α-melanocyte-stimulating hormone on serum levels of LH and prolactin in rats
Authors: Scimonelli T. , Celis M. E. 
Published: December 2008

ABSTRACT
We have investigated the effect of administration of α-MSH into the median eminence (ME) of rats on the release of LH and prolactin.
Continuous infusion of α-MSH (0·5 μg/h) into the ME from the afternoon of the second day of dioestrus and over the 24 h of pro-oestrus inhibited the preovulatory LH and prolactin surge and the occurrence of ovulation. This inhibitory effect on LH and prolactin release was also observed in chronically ovariectomized rats given a single injection of α-MSH (1 μg/μl per rat) into the ME (blood samples were collected 0,20,60,90,105 and 120 min after injection).
The intraperitoneal injection of the dopamine receptor blocker, haloperidol (2 mg/kg), 30 min before the injection of α-MSH into the ME prevented the inhibitory effect of α-MSH on the release of LH and prolactin.
These results suggest that hypothalamic α-MSH might be involved in the regulation of LH and prolactin release via the tuberoinfundibular dopaminergic system and that this system also modifies the serum concentrations of α-MSH.
Journal of Endocrinology (1990) 124, 127–132
Release of oxytocin but not corticotrophin-releasing factor-41 into rat hypophysial portal vessel blood can be made opiate dependent
Authors: Sheward W. J. , Coombes J. E. , Bicknell R. J. , Fink G. , Russell J. A. 
Published: December 2008

ABSTRACT
The effects of morphine dependence and abrupt opiate withdrawal on the release of oxytocin and corticotrophin-releasing factor-41 (CRF-41) into hypophysial portal vessel blood in rats anaesthetized with urethane were investigated. Adult female Sprague–Dawley rats were made dependent upon morphine by intracerebroventricular infusion of morphine for 5 days; abrupt opiate withdrawal was induced by injection of the opiate antagonist naloxone. The basal concentrations of oxytocin in portal or peripheral plasma from morphine-dependent rats did not differ significantly from those in control, vehicle-infused rats. In rats in which the pituitary gland was not removed after stalk section, the i.v. injection of naloxone hydrochloride (5 mg/kg) resulted in a large and sustained increase in the concentration of oxytocin in both portal and peripheral plasma in control and morphine-dependent rats. The i.v. injection of naloxone resulted in a threefold increase in the secretion of oxytocin into portal blood in acutely hypophysectomized rats infused with morphine, but did not alter oxytocin secretion in vehicle-infused hypophysectomized rats. The concentration of oxytocin in peripheral plasma in both vehicle- and morphine-infused hypophysectomized rats was at the limit of detection of the assay and was unchanged by the administration of naloxone. There were no significant differences in the secretion of CRF-41 into portal blood in vehicle- or morphine-infused hypophysectomized rats either before or after the administration of naloxone. These data show that, as for oxytocin release from the neurohypophysis into the systemic circulation, the mechanisms which regulate oxytocin release into the portal vessel blood can also be made morphine dependent. The lack of effect of morphine or naloxone on the release of CRF-41 or other stress neurohormones suggests that the effect of opiate dependence and withdrawal is selective for oxytocin and is not simply a non-specific response to 'stress'.
Journal of Endocrinology (1990) 124, 141–150
Characterization of a tissue kallikrein in human prolactin-secreting adenomas
Authors: Jones T. H. , Figueroa C. D. , Smith C. , Cullen D. R. , Bhoola K. D. 
Published: December 2008

ABSTRACT
Immunoreactive tissue kallikrein was co-localized with prolactin in all the eleven prolactin-secreting adenomas of the human anterior pituitary gland examined in this study. The intracellular distribution of immunoreactivity in the prolactin-secreting cells suggests that tissue kallikrein is located within the Golgi complex of these cells. Both the intracellular hormone-processing action and the kininogenase activity of tissue kallikrein may be of functional importance in human prolactinomas.
Journal of Endocrinology (1990) 124, 327–331
An antioxidant drug, silibinin, modulates steroid secretion in human pathological adrenocortical cells
Authors: Rácz K. , Fehér J. , Csomós G. , Varga I. , Kiss R. , Gláz E. 
Published: December 2008

ABSTRACT
Because human adrenocortical cells from different adrenal disorders exhibit pathologically altered corticosteroid synthesis, and free radical mechanisms may induce pathological changes in the activities of corticosteroid biosynthetic enzymes (cytochrome P-450), we examined the effect of an antioxidant, silibinin, on basal and ACTH-stimulated secretion of several corticosteroids in isolated adrenal cells from an aldosterone-producing adenoma, atrophied adrenal tissues surrounding the adenoma, and hyperplastic adrenals from Cushing's syndrome. In the presence of a high concentration (100 μmol/l) of silibinin, variably diminished secretion of basal aldosterone, corticosterone, cortisol, 18-OH-corticosterone and 11-deoxycorticosterone was found. In contrast, the addition of 0·01 μmol silibinin/l, which failed to produce a clear effect on basal corticosteroid secretion, resulted in a potentiation of ACTH-stimulated secretion of several corticosteroids in the adenomatous and hyperplastic adrenocortical cells. These results suggest that the dose-dependent dual effect of silibinin on corticosteroid secretion may be attributed to corresponding changes in the activities of cytochrome P-450 enzymes, and that stimulation of ACTH-induced corticosteroidogenesis by silibinin is presumably due to the antioxidant property of the drug.
Journal of Endocrinology (1990) 124, 341–345
Growth hormone secretion in the guinea-pig
Authors: Gabrielsson B. , Fairhall K. M. , Robinson I. C. A. F. 
Published: December 2008

ABSTRACT
The guinea-pig is unusual in that it continues to grow at a normal rate after hypophysectomy. Although its pituitary gland appears to contain a GH, this has not been isolated or characterized, and nothing is known about its secretion or physiological control. We have identified guinea-pig GH, established a sensitive heterologous radioimmunoassay and adapted our automatic blood microsampling method to study spontaneous GH secretion in this species. In male guinea-pigs, GH is released in an episodic pattern, reminiscent of the rat. Large multicomponent pulses of GH secretion occur every 3–4 h between periods of low or undetectable GH release, whereas most females showed a more uniform pulsatile pattern with pulses every 1–2 h. GH was released in response to GH-releasing factor (GRF) injections (2, 10 or 20 μg [Nle27]-GRF(1–29)NH2) in a dose-dependent fashion, and i.v. infusion of somatostatin (50 μg/h) blocked spontaneous GH pulses, eliciting a rebound release (from 2·0±0·8 (s.e.m.) to 36±17 μg/l 30 min after stopping the infusion). Infusions of a GH-releasing hexapeptide (100 or 400 μg/h for 4 h) also released GH.
These results provide the first description of the pattern of GH release in the guinea-pig, and suggest that the striking episodic pattern is controlled by the same hypothalamic peptides that regulate GH in other species. Since the guinea-pig grows well in the absence of GH, this species may use GH for its metabolic, rather than growth-promoting actions. The guinea-pig may well prove a useful model, now that methods are available for studying its endogenous GH secretion.
Journal of Endocrinology (1990) 124, 371–380