bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relation between aggressive behaviour and circadian rhythms in cortisol and testosterone in social groups of talapoin monkeys
Authors: Martensz N. D. , Vellucci S. V. , Fuller L. M. , Everitt B. J. , Keverne E. B. , Herbert J. 
Published: December 2008

ABSTRACT
Circadian rhythms in cortisol and testosterone in both blood and cerebrospinal fluid (CSF) were studied in four groups of male and female talapoin monkeys. Samples were taken 4 h apart under two conditions: whilst the sexes were kept separate (isosexual) and again after 24 h of interaction (heterosexual). There were similar rhythms in cortisol in males and females during the isosexual condition, though in blood (but not in CSF) mean levels were higher in females. Heterosexual interaction increased cortisol levels in both sexes (though more so in males), and also altered the shape of the rhythm, acrophase being delayed by 4 h in males and by 2 h in females. The amplitude of the rhythm was not altered. Cortisol levels were positively correlated in both males and females with the amount of aggression received from other males, but not from females nor with the animals' social rank.
Circadian rhythms in serum testosterone in males were also altered by heterosexual interaction. Access to females delayed acrophase by 2 h, but had no effect on mean levels (unlike the effect on cortisol). As for cortisol, the amplitude of the testosterone rhythm remained unchanged. Serum testosterone was negatively correlated with aggression from males, but not from females nor with sexual interaction. This was associated with a pronounced decrease in the levels of testosterone during the night, not observed in males receiving no aggression from others. There was a non-significant trend towards a positive correlation between social rank and serum testosterone.
These results show that social behaviour in groupliving primates has major effects on the parameters of the circadian pattern of secretion of both cortisol and testosterone. Aggression received from males seems to be a potent factor associated with the daily rhythms in both hormones, though there may be rank-related effects in the case of testosterone.
J. Endocr. (1987) 115, 107–120
α-Adrenoreceptor blockade with thymoxamine reduces basal thyrotrophin levels but does not influence circadian thyrotrophin changes in man
Authors: Valcavi R. , Dieguez C. , Azzarito C. , Artioli C. , Portioli I. , Scanlon M. F. 
Published: December 2008

ABSTRACT
We have tested the hypothesis that α-adrenergic drive is involved in the nocturnal increase in TSH in man. Seven mildly hypothyroid women (basal TSH levels 5·0–11·0 mU/1), aged 38–60 years, and nine euthyroid women, aged 27–60 years, were studied. Subjects underwent α-adrenergic blockade by infusion of thymoxamine (210 μg/min from 19.00 to 24.00 h); the same women were used as controls, with saline infused on different nights. Subjects were not allowed to sleep during the study period.
A clear evening rise in basal TSH levels was apparent in both normal subjects and patients. Although overall secretion of TSH was slightly decreased in normal subjects (mean ± s.e.m. area under the curve, 29·93 ± 0·96 vs 30·71 ±mU/1 per h; P<0·05), thymoxamine infusion did not produce any major alteration in the gradual rise in TSH levels during the evening (incremental change above baseline +0·96± 0·21 during control infusion and + 0·97 ± 0·27 mU/1 during thymoxamine infusion). In mildly hypothyroid patients the TSH changes were exaggerated and α-adrenergic blockade caused a reduction in basal TSH levels and a delayed rise in TSH (incremental change above baseline +2·93 ± 1·42 during control infusion and +2·26 ± 0·73 mU/1 during thymoxamine infusion; P < 0·02). Overall TSH secretion was significantly decreased by thymoxamine (mean ± s.e.m. area 106 ± 2·45 mU/1 per h vs 123·32 ± 3·68 in the control study; P<0·0001). As expected, no circadian change was observed in basal prolactin levels in either controls or patients.
Although α-adrenergic pathways may play a role in modulating the nocturnal increase in basal TSH levels, our data suggest that the evening rise in TSH is not a consequence of a primary increase in α-adrenergic drive. The increased TSH changes of mildly hypothyroid patients may, however, be sustained by increased central α-adrenergic stimulation of the TSH secretion.
J. Endocr. (1987) 115, 187–191
Metabolic clearance rate of insulin-like growth factor-I in fed and starved sheep
Authors: Hodgkinson S. C. , Davis S. R. , Burleigh B. D. , Henderson H. V. , Gluckman P. D. 
Published: December 2008

ABSTRACT
The metabolic clearance of insulin-like growth factor-I (IGF-I) has been examined in sheep using a radioiodinated hormone preparation (131I-labelled IGF-I). Following i.v. administration, 131I-labelled IGF-I was distributed in a volume equivalent to plasma (60 ml whole blood/kg liveweight) and demonstrated a triphasic pattern of clearance with apparent half-lives (t½) of 4·0 ± 0·4 (s.e.m.), 52·4 ± 3·4 and 792 ± 26·5 min (n = 10). No significant differences in the t½ of the three phases were identified in fed compared with starved animals (fed, n = 4, phase 1 = 3·1 ± 0·64, phase 2 = 46 ± 5·9 and phase 3 = 756 ± 27 min; starved, n = 6, phase 1 = 4·6 ± 0·58, phase 2 = 57 ± 3·2 and phase 3 = 816 ± 38·5 min). Similarly, no significant differences in the distribution volume (fed, n = 4, 44 ± 4 ml/kg liveweight; starved, n = 6, 39 ± 2 ml/kg liveweight) or metabolic clearance rate (fed, n = 4, 2·9 ± 0·15 ml/min; starved, n = 6, 3·2 ± 0·5 ml/min) of the IGF-I were found in fed compared with starved animals. Highperformance gel filtration chromatography of sequential plasma samples following injection of 131I-labelled IGF-I revealed three clear peaks of radioactivity which demonstrated markedly different patterns of clearance. These correspond to hormone complexed to binding proteins of 150 000 and 50 000 daltons and to 'free' hormone. While radioactivity eluting in the position of free IGF-I had reduced to negligible levels by 12 min, 131I-labelled IGF-I associated with the intermediate molecular weight binding protein was still detectable 6 h after injection. In contrast, an initial increase in radioactivity associated with the 150 000 dalton binding protein was revealed. This form was cleared from the circulation very slowly, by 8 h it was the only species remaining and it was still detectable 26 h after injection. No significant differences in this pattern of bound and free hormone clearance were found in fed compared with starved animals. While there was apparently no interchange of hormone between the binding proteins in vitro the nature of the decay in vivo indicated the possibility of exchange of IGF-I between the different binding proteins.
J. Endocr. (1987) 115, 233–240
Pituitary responsiveness to LHRH during pregnancy in the rat: effect of progesterone
Authors: Koiter T. R. , van der Schaaf-Verdonk G. C. J. , Schuiling G. A. 
Published: December 2008

ABSTRACT
The LH and FSH responses to a standard infusion of LHRH were studied on days 8, 12, 15, 17, 19, 21 and 22 after conception as well as on day 23, i.e. after parturition. Groups of rats were also killed on days 8, 15, 19, 22 and 23 and on the day of pro-oestrus of the 4-day cycle for the assay of progesterone, 20α-dihydroprogesterone (DHP), oestradiol-17β, LH and FSH. Finally, the post-partum surges of LH and FSH were compared with those at pro-oestrus in 4-day cyclic rats.
The LH and FSH responses to LHRH were relatively low on days 8 and 12, twice as high on days 15, 17 and 19, had increased further on day 21 and reached maximal values on day 22. The gonadotrophin responses were low on day 23. The post-partum surges of LH and FSH were much higher than the pro-oestrous surges. Pituitary contents of LH and FSH were higher than on pro-oestrus of the 4-day cycle. On day 23, however, the pituitary contents had declined by 60–80%. No apparent relationship was found between plasma concentrations of LH and FSH and LHRH responsiveness during pregnancy. Concentrations of oestradiol-17β on day 22 were higher than on all other days of pregnancy, but lower than on pro-oestrus of the 4-day cycle. Concentrations of progesterone were high until day 19 and low on days 22 and 23; the concentration of DHP was low until day 19 and very high on days 22 and 23. It was concluded that the increase of the gonadotrophin response to LHRH half-way through pregnancy, in contrast to the increase at the end of pregnancy, cannot be explained by an increase in the concentration of oestradiol-17β, while the pituitary LH and FSH contents play, if any, only a permissive role.
The effect of s.c. implants of progesterone on various hormone parameters during the last week of pregnancy was also investigated. It was found that progesterone not only delayed parturition but also prevented the rise of the gonadotrophin response at the end of pregnancy. Concentrations of oestradiol-17β and DHP were also lower on day 23 than in untreated rats, while the pituitary gonadotrophin contents were higher. It is suggested that delay of luteolysis (in the present study by progesterone treatment) at the end of pregnancy prevents the occurrence of a series of interrelated events: a rise in oestradiol-17β production, a rise in the gonadotrophin responses to LHRH, parturition and the generation of the post-partum gonadotrophin surges.
J. Endocr. (1987) 115, 247–254
The role of calcium and calmodulin in mediating release of thyrotrophin-releasing hormone by cultured hypothalamic cells
Authors: Lewis M. D. , Foord S. M. , Scanlon M. F. 
Published: December 2008

ABSTRACT
We have developed a fetal rat hypothalamic cell culture system for the study of factors controlling the acute release of TRH. Release of TRH by the cells has been characterized by reversed-phase high pressure liquid chromatography and about 86% of the total immunoreactivity in the medium co-eluted with synthetic TRH. Release of TRH by the cells in response to 56 mmol K+/l increased between days 5 and 9 of culture but reached a plateau thereafter. Cell contents of TRH did not change significantly between days 5 and 14 of culture.
Release of TRH from the cells was stimulated by K+ (56 mmol/l), veratridine (100 μmol/l) and ouabain (100 μmol/l) to 550, 480 and 335% of basal release respectively over a 1-h period. Release of TRH was dependent upon calcium in that it was absent when calcium-free medium was used and could be blocked by verapamil (20 μmol/l); however it could not be blocked by nifedipine (50 μmol/l). The calcium ionophore A23187 (1 μmol/l) stimulated TRH release to 340% of basal release. Tetrodotoxin (1 μmol/l) completely abolished the release in response to veratridine but had no effect on the release stimulated by K+ (56 mmol/l).
The calmodulin antagonists trifluoperazine and triflupromazine (50 μmol/l) inhibited veratridine-stimulated TRH release. This was at a site after calcium influx as they also inhibited A23187-stimulated TRH release. The highly specific calmodulin antagonist W7 (10 μmol/l) also inhibited both veratridine and A23187-stimulated TRH release whereas, at the same concentration, its inactive analogue W5 did not significantly inhibit TRH release in response to either stimulus.
These results confirm that fetal rat hypothalamic cell cultures release authentic TRH which can be stimulated by a number of depolarizing agents. Calcium is essential for depolarization-induced release which is also dependent on calmodulin. Fetal rat hypothalamic cell cultures are a valid model for the study of factors controlling the release of TRH.
J. Endocr. (1987) 115, 255–262
Immunoaffinity chromatography of bovine FSH using monoclonal antibodies
Authors: Miller K. F. , Goldsby R. A. , Bolt D. J. 
Published: December 2008

ABSTRACT
Bovine FSH (bFSH) was used to immunize BALB/c mice. Spleen cells were fused to the SP 2/0 cell line to produce hybridomas that secreted monoclonal antibodies to bFSH. One of these antibodies (USDA-bFSH-MC28) was extensively characterized and found to be a gamma 1 with kappa light chains, having extremely low cross-reactivity with other bovine pituitary hormones and with ovine and porcine FSH. The dissociation constant as measured by Scatchard analysis was 4·3 nmol/l, and proved to be in a very useful range for affinity chromatography. In an essentially one-step immunoaffinity chromatography procedure, bFSH was easily isolated in a single chromatographic step from crude anterior pituitary homogenate with better yield and with the same purity as classical chromatographic techniques.
J. Endocr. (1987) 115, 283–288
Alpha1-adrenoceptor production of inositol phosphates mediates the inhibition of thyroxine release from the mouse thyroid
Authors: Muraki T. , Nakaki T. , Kato R. 
Published: December 2008

ABSTRACT
To examine the mechanism of the α1-adrenoceptor-mediated inhibition of the release of thyroid hormones in the mouse thyroid, the effect of noradrenaline on the production of inositol phosphates was investigated using thyroids preloaded with [3H]inositol. Noradrenaline increased [3H]inositol accumulation into inositol phosphates in the mouse thyroid during a 30-min incubation whereas TSH (10 mU/ml) was without effect. The effect of noradrenaline was mimicked by phenylephrine, but not by clonidine or isoprenaline. Prazosin antagonized the effect of noradrenaline, while yohimbine had no effect. These results suggest that noradrenaline-induced production of inositol phosphates is mediated by α1-adrenoceptors. The inhibition of release of thyroid hormones elicited by α1-adrenergic agonists in the mouse thyroid is possibly mediated through the hydrolysis of membrane phosphoinositides followed by the generation of second messengers such as inositol phosphates and diacylglycerol.
J. Endocr. (1987) 115, 289–293
Studies of the rapid effects of parathyroid hormone and prostaglandins on 45Ca uptake into chick and rat bone in vivo
Authors: Dacke C. G. , Shaw A. J. 
Published: December 2008

ABSTRACT
The rapid effects of parathyroid hormones and a variety of prostaglandins on net uptake of 45Ca into the skeleton have been investigated in chicks and, in a limited parallel study, in immature rats.
Intravenous injection of bovine (b) parathyroid hormone(1–34) bPTH(1–34)) or 16,16-dimethyl prostaglandin E2 (16,16-dimethyl PGE2) in a 45Ca-labelled vehicle, combined with subsequent microwave fixation of tissue isotope levels, resulted in rapid (3–15 min) net inhibition of 45Ca uptake into endochondral bone (femur) in chicks (12 days old) and rats (4 weeks old). Use of 125I-labelled albumin and [14C]mannitol indicated that these responses were not a reflection of gross changes in tissue vascular or extracellular space. In rats, bPTH(1–84) also caused significant net inhibition of 45Ca uptake into femur at 10 min. Both bPTH(1–34) and 16,16-dimethyl PGE2 produced generally smaller decreases in 45Ca uptake into chick dermal bone (calvarium) at 3–15 min. In rat calvarium, however, these agents stimulated net uptake of 45Ca at these times. When microwave fixation was omitted, inhibitory responses were reduced or disappeared, while the stimulatory response in rat calvarium was enhanced. Responses to natural prostaglandins (PGE1, PGE2, PGF2α and PGI2) in chicks at 3 min were similar but less marked than those to 16,16-dimethyl PGE2; 45Ca uptake into femur and, to a lesser extent in calvarium, being inhibited. In rats, PGE1, PGE2 and PGF2α showed a tendency to decrease 45Ca uptake into femur while PGE1 and PGE2 both increased 45Ca uptake into calvarium.
J. Endocr. (1987) 115, 369–377
Difference in luteal and placental P45017α: substrate preference and hormonal regulation in the rat
Authors: Eckstein B. , Khan I. , Gibori G. 
Published: December 2008

ABSTRACT
The purpose of this study was to assess the substrate specificity of P45017α in both the corpus luteum and placenta of pregnant rats, and to analyse the site at which LH/human chorionic gonadotrophin (hCG) regulates the activities of this enzyme. To distinguish the substrate preference, placentas and corpora lutea were obtained from rats on day 15 of pregnancy. Tissues were homogenized and the 10 000 g supernatants incubated in the presence of equimolar concentrations of [14C]progesterone and [3H]17α-hydroxyprogesterone as substrate with either NADH or NADPH as cofactors for 2, 8, 16 and 24 min. The labelling pattern of both 17α-hydroxyprogesterone and testosterone indicated that the corpus luteum produced testosterone preferentially from progesterone, whereas the placenta principally used 17α-hydroxyprogesterone and synthesized six times as much testosterone from 17α-hydroxyprogesterone than from progesterone. Addition of either NADPH or NADH as cofactors had no effect on substrate preference. The products of the two enzymatic activities were identified by recrystallization to constant 14C/3H ratios. The ratio of 14C/3H in testosterone produced by the corpus luteum was 16-fold higher than in that produced by the placenta. To explore which of the two activities of P45017α is regulated by the gonadotrophin, rats were treated with either 1·5 IU hCG or vehicle between days 13 and 15 of pregnancy. Hydroxylase and lyase activities were determined on day 15 after incubation for 2,8,16 or 24 min in the presence of either NADH or NADPH. Administration of hCG significantly inhibited NADH-dependent 17α-hydroxylase in the placenta at each time-point studied. The inhibition reached 69% at 24 min. Human chorionic gonadotrophin did not affect the NADPH-dependent 17α-hydroxylase and had only a slight inhibitory effect on both NADH- and NADPH-dependent 17,20-lyase activities in the placenta. In contrast to its effect on the placenta, hCG stimulated both NADH- and NADPH-linked 17,20-lyase activities but had no measurable effect on 17α-hydroxylase activities in the corpus luteum.
In summary, the results of the present investigation have revealed a significant difference in the behaviour of 17α-hydroxylase/17,20-lyase activities in the placenta and corpus luteum. The substrate preference and the control of both enzyme activities by LH/hCG differs dramatically.
J. Endocr. (1987) 115, 387–393
Mechanism of replenishment of androgen receptors in cytosol of mouse submandibular gland
Authors: Kyakumoto S. , Kurokawa R. , Ota M. 
Published: December 2008

ABSTRACT
Female mice were used to examine the process of depletion and replenishment of cytosolic androgen receptors in submandibular glands, and to investigate the effects of cycloheximide and actinomycin D on these processes. The dose-dependence of receptor depletion and replenishment in the cytosolic fraction, and that of receptor accumulation in the nuclear fraction were investigated. Almost 100% depletion was revealed 1 h after the injection of testosterone propionate at a dose of 500 or 50 μg testosterone/100 g body weight. With a 5 μg dose, depletion of cytosolic receptors was not complete and replenishment proceeded rapidly compared with that which occurred with the 50 or 500 μg dose. The nuclear receptor level increased 1 h after injection of testosterone, and the raised level was gradually reduced to the pretreatment level with all doses. However, the time required for this return to pretreatment level was dependent on the dose of testosterone. The change in the levels of cytosolic and nuclear androgen receptors following injection of testosterone was parallel to the level of circulating androgen. To determine the requirements for transcriptional and translational events in the replenishment process, cycloheximide and actinomycin D were given in vivo. The process of replenishment of cytosolic receptors was inhibited by the injection of cycloheximide. However, actinomycin D exerted no inhibitory effect on receptor replenishment. Neither cycloheximide nor actinomycin D had any effect on the nuclear receptor level until 6 h after the injection of testosterone. Cycloheximide or actinomycin D alone had no effect on the cytosolic or nuclear receptor level. These results suggest that receptor replenishment involves protein synthesis.
J. Endocr. (1987) 115, 411–418
Dopamine stimulates release of thyrotrophin-releasing hormone from perfused intact rat hypothalamus via hypothalamic D2-receptors
Authors: Lewis B. M. , Dieguez C. , Lewis M. D. , Scanlon M. F. 
Published: December 2008

ABSTRACT
We have studied the effect of dopamine together with agonist and antagonist drugs of different specificities on the release of TRH from the perfused, intact hypothalamus of the adult rat in vitro. Dopamine produced a dose-related stimulatory effect on TRH release with maximal effect being achieved at 1 μmol/l (increase over basal, 118 ±16·5 (s.e.m.) fmol TRH; P <0·001 vs basal). This effect was mimicked by the specific D2-agonist drugs bromocriptine (0·1 μmol/l) and LY 171555 (0·1 μmol/l) (increase over basal values, 137·5±13·75 fmol and 158·6± 10·7 fmol respectively; P <0·001 vs basal), but not by the D1-agonist SKF 38393A. The stimulatory effect of dopamine (1 μmol/l) was blocked in a stereospecific manner by the active (d) but not by the inactive (l) isomers of the dopamine antagonist butaclamol. Similar blockade was achieved with the specific D2-antagonist domperidone (0·01 μmol/l) whereas the D1-antagonist SCH 23390 was only effective when used at a concentration 100 times greater. Lower concentrations (0·01 μmol/l) of this D1 -antagonist did not block the stimulatory effect of dopamine. High-performance liquid chromatography characterization of the material secreted within the hypothalamus showed one single peak of immunoreactive material which coeluted with synthetic TRH. These data suggest that dopamine exerts a stimulatory role in the control of hypothalamic TRH release by acting at specific D2-receptors.
J. Endocr. (1987) 115, 419–424