bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pyridostigmine, an Acetylcholinesterase Inhibitor, Stimulates Growth Hormone Release, but has no Effect on Basal Thyrotrophin or Adrenocorticotrophin Levels, or the Thyrotrophin Response to Thyrotrophin‐Releasing Hormone
Authors: Freeman Emma , Touzel Rick , Grossman Ashley , Besser Michael , Ross Richard 
Published: September 2006

AbstractPyridostigmine, an acetylcholinesterase inhibitor, stimulates growth hormone (GH) release and is thought to act by inhibiting hypothalamic somatostatin release. There are few data concerning the effect of pyridostigmine on other pituitary hormones apart from GH. We have studied the effect of pyridostigmine on basal GH, thyrotrophin (TSH), prolactin, adrenocorticotrophin and cortisol release, and thyrotrophin‐releasing hormone (TRH)‐stimulated TSH and prolactin release, in two studies involving nine healthy male subjects. Pyridostigmine stimulated GH release in all subjects but had no effect on adrenocortocotrophin or cortisol levels, or basal or TRH‐stimulated TSH and prolactin levels.There are some data to suggest that somatostatin inhibits TRH‐stimulated TSH release. Our findings, however, suggest that either endogenous somatostatin tone has little effect on the TSH response to TRH compared to its effects on GH or pyridostigmine acts through a mechanism other than altering somatostatin tone. Pyridostigmine did not alter adrenocorticotrophin or cortisol levels in the presence of a clear action on GH release, providing further evidence that the previously reported effects of cholinergic drugs on cortisol release are stress‐related.
Ovarian Steroid Regulation of Glutamic Acid Decarboxylase Gene Expression in Individual Hypothalamic Nuclei
Authors: Leigh A J. , Carter N.D. , Horton R. , Silverligh J.J. , Wilson C.A. 
Published: September 2006

AbstractThe possibility that steroids exert their effects on luteinizing hormone (LH) and prolactin release and female sexual behaviour via altering γ‐aminobutyric acid (GABA) synthesis within the hypothalamus was investigated. Ovariectomized rats were treated with either oil, 5 μg oestradiol benzoate (OB) or 5 μg OB plus 0.5 mg progesterone (P) 48 h later; autopsy was carried out 54 h after the OB injection. At this time, both steroid treatments stimulated prolactin release and lordotic activity. OB alone exerted a negative feedback effect on LH release while OB plus P stimulated an LH surge.The brains of the rats in these three treatment groups were microdissected and glutamic acid decarboxylase messenger nbonucleic acid (GAD mRNA) was estimated in specific hypothalamic areas obtained from individual brains; these areas included the preoptic area (POA), ventromedial nucleus (VMN), anterior medial portion of the zona incerta (Zl) and the arcuatemedian eminence area (ARC/ME). GAD mRNA concentrations were assessed by the slot‐blotting technique and expressed as a ratio of GAD mRNA: β‐actin mRNA.Both steroid treatments significantly reduced GAD mRNA in the ARC/ME and Zl and OB plus P also reduced the concentration in the POA, while OB alone had no effect in this area. Neither treatment affected GAD mRNA in the VMN. These results indicate that when steroids stimulate LH and prolactin release and female sexual behaviour, they reduce GABA activity probably by reducing GABA synthesis in the POA, Zl and ARC/ME. This suggests that GABA normally has an inhibitory influence on these parameters. GABA synthesis does not however, appear to be involved in the negative feedback effects of steroids on LH release as measured 54 h after OB treatment.
Release of Vasopressin from the Septum and Hippocampus of Freely Behaving Male Rats: Effect of Bacitracin and Synthetic Vasopressin
Authors: Ramirez V. D. , Ramirez A. D. , Rodriguez F. , Poncett C. , Vincent J. D. 
Published: September 2006

AbstractThis paper describes the release characteristics of arginine vasopressin (AVP) from the dorsal septum and dorsal hippocampus of freely behaving male rats using miniaturized push‐pull cannulae and a slow rate of perfusion to minimize tissue damage. The major findings were that) The spontaneous release of immunoreactive AVP (l‐AVP) from the dorsal hippocampus was episodic in nature and did not require the presence of bacitracin in the perfusion medium to reliably demonstrate its pattern of release; 2) despite the fact that the septum has close to seven times more I‐AVP per/mg of tissue, the dorsal septum perfusates had undetectable levels of the neuropeptide; 3) under these conditions hypertonic saline intraperitoneally did not alter the spontaneous release of this peptide; and 4) only when the perfusion medium contained effective concentrations of bacitracin (10−4 M) were reliable and detectable levels of I‐AVP measured in perfusates from the dorsal septum and exogenous synthetic AVP had a robust positive feedback action on its own release. The physiological relevance and importance of this robust and novel effect of AVP remains to be elucidated.
Effects of Alpha‐ and Beta‐Adrenergic Agonists and Antagonists on Growth Hormone Secretion in Man
Authors: Ghigo E. , Bellone J. , Arvat E. , Mazza E. , Cellat S. G. , Brambilla F. , Müller E. E. , Camanni F. 
Published: September 2006

AbstractIt is well known that the adrenergic system has both stimulatory and inhibitory influences on growth hormone (GH) secretion probably by modulating GH‐releasing hormone (GHRH) and/or somatostatin release. To better understand the mechanisms by which these influences take place, we investigated the effects of α‐ and β‐adrenergic agonists and antagonists on both basal and GHRH‐induced GH release in 23 male adult volunteers. The GH‐releasing effect of clonidine (0.15 mg infused iv over 10 min), an α2‐adrenergic agonist, was significantly blunted by yohimbine (30 mg orally at −50 min), a relatively specific α2‐adrenergic antagonist area under the response curve, mean±SEM: 672.6 ± 143.0 versus 219.6 ± 16.7 μg/l/h; P<0.05). On the other hand, the GHRH (1 μg/kg iv as a bolus)‐induced GH increase was unaffected by yohimbine (339.3 ± 19.1 versus 518.1±172.8 μg/I/h). Concomitant blockade of α1‐/α2‐adrenoreceptors by phentolamine (0.5 mg/ml/min infused iv from −60 to +30 min) abolished the GHRH‐induced GH rise (645.5± 106.0 versus 189.0±58.8 μg/l/h; P<0.01). Finally, the GHRH‐stimulated release was blunted by β2‐adrenergic stimulation with salbutamol (10 μg/min infused iv from −5 to +15 min) (324.3 ± 99.7 versus 112.7 ± 48.8 μg/l/h; P<0.02).In conclusion: 1) The evidence that yohimbine is able to blunt the clonidine‐induced GH release but fails to inhibit the GHRH‐induced GH rise indicates that, as in animals, in man too the GH‐releasing effect of clonidine is specifically mediated by α2‐receptor activation, and may occur via endogenous GHRH release; 2) the inhibitory effect on GH release of β, namely β2, receptor activation is probably mediated by the somatostatinergic system; 3) an unopposed β‐adrenergic activation would account for the inhibitory effect on GHRH‐induced GH release of concomitant α1–/α2‐adrenoreceptor blockade by phentolamine.
The Possible Role of Androgenic Hormones in Maturation of Alpha2‐Adrenergic Mechanisms in the Rat
Authors: Kiem D. T. , Bartha L. , Makara G. B. 
Published: September 2006

AbstractIn order to get better characterization of androgenic hormones on the functionality of the α2‐adrenergic system and widen our previous studies, we investigated the effect of clonidine on the growth hormone (GH) secretion in male Wistar rats of various ages: 7‐, 14‐ and 30‐day old and adult, adult male castrated rats with and without testosterone treatment.Two different patterns of the GH response to clonidine have been observed in the control and testosterone‐treated young animals: clonidine at the dose 15 μg/kg intraperitoneally had no effect on the GH secretion in 7‐ to 14‐day old rat pups. In contrast, its effect appeared following the increase in the plasma testosterone concentration induced by pretreatment with testosterone (5 mg/kg subcutaneously for 4 days) in these animals. In 30‐day old rats clonidine affected GH secretion and this influence was more pronounced in the testosterone‐treated animals than in the controls.The decrease in the circulating testosterone levels caused by castration in adult male rats caused a decreased GH response to clonidine. Moreover, there was a tendency for the GH response to return in 4‐week old animals. The effect of clonidine has been restored by testosterone replacement of castrates.Testosterone administration decreased basal plasma GH levels in the pups. However, it triggered the ultradian surges of GH secretion which were absent in the young animals.Clonidine had no effect on the corticosterone secretion in 7‐day old animals. Testosterone treatment induced a response in the 7‐day old rat and markedly potentiated its effect on the secretion of this hormone in 14‐ and 30‐day old animals, respectively.Neither progesterone nor hydrocortisone influenced the GH‐releasing effect of clonidine. Hydrocortisone markedly inhibited the basal‐ and clonidine‐induced corticosterone secretion.The results of the present study indicate an important role of androgenic hormones in inducing and/or maintaining the effectiveness/sensitivity of the α2‐adrenergic receptor system and suggest a possible role for the androgenic hormones in the maturation of α‐adrenergic mechanisms in the rat.
Regional Changes in Brain Oxytocin Receptors Post‐Partum: Time‐Course and Relationship to Maternal Behaviour
Authors: Insel Thomas R. 
Published: September 2006

AbstractIn a previous report, receptors for oxytocin in rat brain were reported to increase during the early post‐partum period. The current study set out to replicate this finding using the novel, highly selective oxytocin receptor ligand, [125 l]d(CH2)5[Tyr(Me)2, Thr4, Tyr‐NH29]OVT ([125 I]‐OTA). Binding was measured using in vitro receptor autoradiography in rat brain on Day 15 of pregnancy, on Days 1 and 6 post‐partum, and at least 6 days following the end of lactation. Relative to pregnancy, oxytocin receptor binding was increased on Day 1 (but not Day 6) post‐partum in the bed nucleus of the stria terminalis and the ventromedial nucleus of the hypothalamus. In several other regions, including the anterior olfactory nucleus, the central nucleus of the amygdala, and the ventral subiculum binding was equivalent across the groups. Most surprising, binding in the bed nucleus of the stria terminalis was lowest in the post‐lactating group (post‐partum Day 1 group was 87% higher than post‐lactating group). Saturation studies suggested that binding differences reflected changes in number and not affinity of sites. These findings are consistent with earlier studies of changes in brain oxytocin receptors following exogenous gonadal steroid administration. To determine if maternal behaviour elicited by nonhormonal means (i.e. concaveation) was also associated with increased oxytocin receptors, virgin females with extensive pup exposure were studied. No change in oxytocin receptor binding in the bed nucleus of the stria terminalis was noted in virgin, maternal females—demonstrating that the increase observed post‐partum was not essential for the onset of maternal behaviour.
Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin
Authors: Sato Makoto , Takahara Jiro , Niimi Michio , Irino Shozo 
Published: September 2006

AbstractThe episodic pattern of growth hormone (GH) secretion of the male rat was simulated in rats exhibiting impaired GH‐releasing factor (GRF) and Somatostatin (SRIF) secretion, by administering various combinations of human GRF‐(1–44)NH2 (hGRF) and SRIF. Electrical lesions of the arcuate nucleus resulted in a marked decrease in the amplitude of GH secretory bursts, while the administration of cysteamine (200 mg/kg) did not change the GH secretory profile in rats with arcuate nucleus lesions. Immunohistochemical examinations revealed a marked decrease of GRF and SRIF immunoreactivity in the median eminence of the cysteamine‐treated rats with arcuate nucleus lesions. The intravenous injection of 5 μg of hGRF every 3 h caused equivalent surges of GH in the cysteamine‐treated rats with arcuate nucleus lesions. The additional infusion of 4 μg/h of SRIF during the trough periods of GH secretion did not affect the amplitude of the GH surges. Hourly injection of 5 μg of hGRF caused transient desensitization to hGRF. Interestingly, the additional infusion of 4 μg/h of SRIF every 3 h enhanced the amplitude of the GH bursts induced by the fourth and the seventh hGRF injections. However, the more frequent injection of 5 μg of hGRF every 30 min caused constant desensitization to hGRF with time, and the additional infusion of 4 μg/h of SRIF every 3 h did not change the attenuated responses to hGRF. These results indicated that the simultaneous administration of hourly GRF and continuous SRIF with brief pauses was most effective for producing high GH peaks. This simulation model suggests that SRIF may play an important role not only in the production of GH troughs, but also in the maintenance of GH surges with distinct peaks in the male rat.
Pituitary Hormone Gene Expression in Male Golden Hamsters: Interactions Between Photoperiod and Testosterone
Authors: Hegarty Catherine M. , Jonassen Julie A. , Bittman Eric L. 
Published: September 2006

AbstractDaylength regulates neuroendocrine function in male golden hamsters. Exposure to short days triggers gonadal regression and decreases serum luteinizing hormone (LH), prolactin and testosterone concentrations. Inhibitory photoperiods also amplify the negative feedback actions of androgens upon gonadotropin secretion. To examine whether these changes arise from altered adenohypophyseal gene expression, we measured the abundance of the messenger ribonucleic acids (mRNAs) encoding β‐LH, prolactin and proopiomelanocortin in anterior pituitaries of male golden hamsters which were either left intact, castrated, castrated and implanted with testosterone, or pinealectomized and maintained in either long (14 h light/10 h dark) or short (5 h light/19 h dark) days. Short days caused testicular atrophy in intact male hamsters and reduced serum LH in intact and castrated, testosterone‐replaced hamsters. The relative abundance of β‐LH mRNA was suppressed by exposure to short days only in castrated hamsters. Serum prolactin was decreased by short days regardless of circulating testosterone concentrations. Prolactin mRNA abundance was decreased by short days in all pineal‐intact groups. Castration reduced proopiomelanocortin mRNA abundance in long days and testosterone replacement reversed this effect. In the presence of testosterone, photoperiod influenced serum LH concentrations without altering hypophyseal abundance of β‐LH mRNA. In contrast, photoperiodic influences on prolactin secretion were correlated with alterations in steady‐state mRNA abundance.
Ontogenesis and Sexual Dimorphism of Rat Growth Hormone Messenger Ribonucleic Acid as Studied by in situ Hybridization
Authors: Martinoli M. G. , Pelletier G. 
Published: September 2006

AbstractWe have investigated the ontogeny of growth hormone (GH) mRNA in the developing rat foetus and also from birth to adulthood. Using quantitative in situ hybridization, we studied the variations in the levels of GH mRNA during foetal and postnatal life in the pituitary of both male and female rats. A cDNA probe to GH mRNA was used to detect GH transcripts on fixed pituitary sections at different stages of development. Few labelled cells were observed in the lateral wings of the anterior pituitary from the 17th to 19th day of gestation in both sexes. The amounts of GH mRNA significantly increased in both male and female rats from neonatal to adult life, reaching the highest levels after puberty. A clear sexual dimorphism was observed at the 20th day of foetal life, GH mRNA levels being higher in male than in female rats. After birth, no significant differences of GH mRNA levels could be observed between male and female rats until 30 days of age (prepubertal period) when male rats exhibited GH mRNA levels higher than females. This sexual difference in GH mRNA levels remained constant throughout adult life. Moreover, gonadectomy performed at neonatal, prepubertal and adult periods in both male and female rats did not modify GH mRNA levels in either sex. These results indicate that an early synthesis of GH mRNA occurs in foetal pituitary and that the sexual dimorphism of GH mRNA observed from 30 days of age is not related to sex steroids.
Oxytocin Messenger Ribonucleic Acid Levels in the Medial Preoptic Area are Increased During Lactation
Authors: Brooks Philip J. , Lund P. Kay , Stumpf Walter E. , Pedersen Cort A. 
Published: September 2006

AbstractThe peptide hormone oxytocin has an important role in parturition, lactation and maternal behavior. The present study employed in situ hybridization histochemistry to determine whether oxytocin messenger ribonucleic acid (mRNA) levels in cells in the medial preoptic area, a brain area known to control maternal behavior, change during pregnancy and lactation in the rat. Female rats were perfused on either Day 18 or 22 of pregnancy or Day 5 of lactation. Ovariectomized female rats were included as an additional control group. Cells expressing oxytocin mRNA were detected by in situ hybridization using an [125 l]‐labeled 38 base synthetic oligodeoxynucleotide probe complementary to the C‐terminal coding region of the preprooxytocin. Relative differences in oxytocin mRNA levels were determined by silver grain counting of labeled cells. A group of oxytocin neurons in the dorsal medial preoptic area, called the lateral subcommissural nucleus, showed elevated oxytocin mRNA levels in lactating animals relative to ail other groups. Oxytocin mRNA levels in the neurons of the periventricular nucleus of the preoptic area did not change across pregnancy and lactation. This result extends the findings of others showing elevated oxytocin mRNA levels in magnocellular nuclei of lactating animals. The results are discussed in terms of the possible role of oxytocin cells in the medial preoptic area in the expression of maternal behavior.
N‐Methyl‐DL‐Aspartate Receptor Antagonism by D‐2‐Amino‐5‐Phosphonovaleric Acid Delays Onset of Puberty in the Female Rat
Authors: Wu F. C. W. , Howe D. C. , Naylor A. M. 
Published: September 2006

AbstractTo investigate the possible role of N‐methyl‐DL‐aspartate (NMDA) receptor activation in the initiation of puberty, we examined the effects of the selective competitive antagonist 2‐amino‐5‐phosphonovaleric acid (AP5) on the timing of vaginal opening. Paired and weight‐matched litter mates of immature female rats were implanted with osmotic minipumps for the intracerebroventricular infusion of DL‐ or D‐AP5 or artificial cerebrospinal fluid from 27 to 30 days of age for 14 days. Each animal was weighed and examined daily for vaginal opening as the indicator of first oestrous. Infusion of 20 or 40 mM DL‐AP5 beginning on Day 30 failed to delay vaginal opening. Administration 50mM of the single enantiomer D‐AP5 beginning on Day 27 significantly delayed the age of vaginal opening to 40.6±1.1 (mean ± SEM) days compared to the cerebrospinal fluid‐infused controls (36.5 ± 0.6 days). Blockade of NMDA receptors in the D‐AP5‐treated animals was confirmed on Day 32 by the suppression of luteinizing hormone response to intravenous NMDA (20 mg/kg) while the response to exogenous luteinizing hormone‐releasing hormone (50 ng/kg) remained intact. AP5‐treated animals had a slower rate of growth (3.1 ± 0.2 g/day) compared to controls (4.2 ± 0.2 g/day). However, a similar degree of growth retardation produced by a 75% restricted diet in untreated juvenile animals did not delay vaginal opening. This suggests that the slower growth rate in the D‐AP5‐treated animals could not account for the delayed onset of puberty. In conclusion, these data suggest that blockade of central NMDA receptors inhibits excitatory mechanisms which may be important in the control of pubertal onset in the female rat.
Regulation of the Rat Oxytocin Gene by Estradiol
Authors: Peter J. , Burbach H. , Adan Roger A. H. , van Tol Hubert H. M. , Verbeeck Marleen A. E. , Axelson John F. , van Leeuwen Fred W. , Beekman Johanna M. , Ab Geert 
Published: September 2006

AbstractOxytocin (OT) plays a role in reproduction at the level of the pituitary and mammary glands and uterus. This OT is synthesized in the hypothalamo‐neurohypophyseal system (HNS). A number of observations have suggested that estrogens regulate the production of OT in the HNS. In this study the effect of 17β‐estradiol on the activity of the OT gene promoter was examined as well as the effect of 17β‐estradiol in vivo on OT messenger ribonucleic acid (mRNA) and peptide revels in the rat HNS. Vasopressin (VP) and its mRNA were also determined in the in vivo studies. The direct transcriptional stimulation of OT gene expression by 17β‐estradiol was studied in two different heterologous expression systems. When a plasmid having nucleotides −363 to +16 of the rat OT gene fused to the firefly luciferase reporter gene was co‐transfected with an estrogen receptor expression vector in P19 embryonal carcinoma cells, luciferase activity was stimulated 80‐fold by 17β‐estradiol. In estrogen receptor containing MCF‐7 cells transfected with a plasmid having nucleotides −188 to +16 of the rat OT gene fused to the chloramphenicol acetyl transferase gene, 17β‐estradiol induced the expression of the chloramphenicol acetyl transferase gene through the cloned promoter element. After in vivo treatment of ovariectomized rats with 17β‐estradiol, levels of OT mRNA and VP mRNA were measured in microdissected supraoptic and paraventricular nuclei as well as VP and OT levels in these nuclei and the pituitary gland. As compared to non‐treated ovariectomized rats there was no difference in contents of OT mRNA and VP mRNA in these hypothalamic nuclei and in levels of the peptides in paraventricular nuclei and the pituitary gland. A 30% reduction of the OT content of the supraoptic nuclei only was found, while the VP content did not change. To explain the results immunocytochemical analyses of the hypothalamus were performed, showing that the estrogen receptor was absent in the magnocellular neurons of the supraoptic and paraventricular nuclei. The results demonstrate that the 5’flanking region of the OT gene confers estrogen‐sensitivity to transcription of the OT gene. This potential to respond to estrogens is not used in the OT‐producing neurons of supraoptic and paraventricular nuclei probably due to the absence of the estrogen receptor.
Immunocytochemical Localization of Glucagon‐Related Peptides in the Cerebral Ganglion of the Protochordate Ascidian, Styela plicata
Authors: Pestarino Mario 
Published: September 2006

AbstractThe central nervous system of the protochordate ascidian Styela plicata has been investigated by means of immunocytochemical techniques in order to localize peptides of the glucagon/secretin family. In particular, glucagon‐ and peptide histidine isoleucine‐containing neurons were localized in the cortex of the cerebral ganglion, and numerous nerve cell bodies containing vasoactive intestinal polypeptide occurred mainly in the medullary zone. Moreover, coexistence of glucagon/peptide histidine isoleucine and glucagon/vasoactive intestinal polypeptide was detected in a few cortical neurons. The localization of peptide histidine isoleucine‐like peptides in the central nervous system and alimentary tract supports the occurrence of a ‘brain‐gut axis’ in protochordates as well as in vertebrates and some invertebrates, while glucagon‐ and vasoactive intestinal polypeptide‐like substances can be considered exclusively as neuropeptides.