bluuebunny/crossref_metadata_2025_split huggingface dataset:
Somatostatin and Thyrotrophin‐Releasing Hormone Response and Receptor Status of a Thyrotrophin‐Secreting Pituitary Adenoma: Clinical and in vitro Studies
Authors: Levy Andrew , Eckland David J. A. , Gurney Alison M. , Reubi Jean‐Claude , Doshi Rasikbala , Lightman Stafford L. 
Published: September 2006

AbstractWe have described a patient with a thyrotrophin‐secreting pituitary adenoma and correlated a detailed physiological and anatomical investigation of the surgically resected tumour with its in vivo regulation. Thyrotrophin secretion was inhibited by circulating thyroid hormones, dopaminergic agonists and the somatostatin analogue SMS 201–995 but could not be stimulated by thyrotrophin‐releasing hormone or further inhibited by exogenous triiodothyronine. Prolonged treatment with SMS 201–995 caused tumour shrinkage as shown by successive computed tomography scans but was accompanied by tumour desensitization and the development of diabetes mellitus. This is the first thyrotroph adenoma in which somatostatin receptors have been directly demonstrated and shown to completely block thyrotrophin‐releasing hormone‐induced inositol phospholipid accumulation when occupied. In addition, preincubation with triiodothyronine significantly inhibited thyrotrophin‐releasing hormone‐induced inositol phospholipid turnover in dispersed pituitary cells indicating that in this tumour, circulating thyroid hormones were exerting feedback inhibition at the level of the pituitary either by reducing the number of thyrotrophin‐releasing hormone receptors and/or their coupling to second messenger pathways. In keeping with this hypothesis, the acute reduction in intrapituitary triiodothyronine by sodium ipodate in vivo had no effect on peripheral thyrotrophin over 6 h suggesting that the onset of the effect of triiodothyronine withdrawal on thyrotrophin secretion was suitably delayed. The importance of the inositol phospholipid second messenger pathway in transducing the secretory response in this tumour was further corroborated by electrophysiological studies which demonstrated thyrotrophin‐releasing hormone‐induced changes in K+ currents which are dependent on intracellular Ca2+ ions, presumably mobilized via the inositol phospholipids. In addition to thyrotrophin and α subunit, growth hormone mRNA and growth hormone were found throughout the tumour as were two populations of cells distinguished electron microscopically by the size of their secretory granules. Although acromegalic features are not unusual in thyrotroph adenomas, our patient showed no evidence of inappropriate growth hormone secretion during surgery or in response to pre‐ or post‐operative insulin stress tests.
A Small Population of Tyrosine Hydroxylase‐lmmunoreactive Neurons in the Guinea‐Pig Arcuate Nucleus Contains Progestin Receptor‐lmmunoreactivity
Authors: Blaustein Jeffrey D. , Turcotte Joanne C. 
Published: September 2006

AbstractWe studied the co‐localization of progestin receptor‐immunoreactive (PR‐IR) cell nuclei and tyrosine hydroxylase‐immunoreactive (TH‐IR) cell bodies in guinea‐pig brain with a double antibody, immunocytochemical technique. Sections were first immunostained for estradiol‐induced PR‐IR using a peroxidase‐antiperoxidase technique with diaminobenzidine as the chromogen followed by α‐naphthol as the chromogen for TH‐IR. We examined the periventricular‐preoptic area and the arcuate nucleus, because these two sites are dense in both PR‐IR cells and TH‐IR cells (cell groups A14 and A12, respectively), and the dorsal hypothalamic Area A13, because this area contains a high density of TH‐IR cells, but few PR‐IR cells. No co‐localization was seen in the periventricular‐preoptic area or Area A13. However, a small proportion (5% to 13%) of TH‐IR cells in the arcuate nucleus was observed to have PR‐IR cell nuclei with the rostral arcuate showing the greatest concentration of co‐localized cells. In order to determine if the estradiol pretreatment required to induce PR‐IR influenced TH‐IR, TH‐IR in estradiol‐primed guinea‐pigs was compared with that of vehicle‐injected controls. This treatment did not noticeably influence the amount of TH‐IR in the arcuate nucleus. Therefore, the results of these experiments suggest that, although some of the TH‐IR neurons in the arcuate nucleus contain PR‐IR, this relationship is seen in less than 15% of the TH‐IR cells. In many cases, PR‐IR neurons were found to have TH‐IR varicosities closely associated with their cell bodies.
Spinal Arginine Vasopressin Elevates Renal Nerve Activity in the Rat
Authors: Riphagen Colleen L. , Pittman Quentin J. 
Published: September 2006

AbstractIntrathecal injections of arginine vasopressin increased activity recorded from multifiber renal nerve bundles of anesthetized rats by 47 + 14%. This response was significantly attenuated following perfusion of the intrathecal space with a vasopressin antagonist, d(CH2)5Tyr(Me)AVP. It is unlikely that vasopressin leaked to the periphery as iv administration of 10 pmol vasopressin decreased renal nerve activity by 9 + 1%. Electrical stimulation of the paraventricular nucleus (three stimuli at 20 to 100 μA, 100 or 200 Hz) caused a biphasic excitatory response with the peaks of increased renal nerve activity occurring between 50 to 100 and 100 to 200 ms after stimulation. Intrathecal application of the vasopressin antagonist prior to repeating the stimulation of the paraventricular nucleus attenuated the second excitatory response without affecting the first excitatory episode. In animals in which the stimulating electrode was located adjacent to, but not within, the paraventricular nucleus, a monophasic excitatory response (at between 100 to 150 ms after the stimulation) was observed. This response was not attenuated by the intrathecal antagonist. These results are consistent with earlier studies which suggested that arginine vasopressin may function as a mediator of synaptic transmission at spinal levels in pathways influencing kidney function.
Stress‐Related Changes in β‐Endorphin Processing: The Limitations of Slaughterhouse Material
Authors: Smith A. Ian , Wallace Catherine A. , Clarke Lain J. , Funder John W. 
Published: September 2006

AbstractIn the sheep, unlike many other species, a significant proportion (>25%) of immunoreactive β‐endorphin in the anterior pituitary is post‐translationally modified to opioid‐inactive, α‐N‐acetylated forms. In a study to determine the precise molecular nature of α‐N‐acetylated β‐endorphin immunoreactivity, we noted a striking difference in high‐performance liquid chromatography profiles of anterior pituitary extracts between sheep killed on the farm, and age‐, sex‐ and strain‐matched slaughterhouse animals. These altered patterns of a‐N‐acetylated β‐endorphin processing were reproduced in farm animals by chronic (≤ 4 days) treatment with the synthetic glucocorticoid dexamethasone; in contrast dexamethasone had no effect on a‐N‐acetylated β‐endorphin processing in hypothalamo‐pituitary disconnected sheep. These data suggest that (1) the change in processing is a stress response, mediated by prolonged glucocorticoid exposure, (2) this effect is central, rather than a direct effect on the pituitary, and (3) the relative abundance of various peptide sequences in slaughterhouse‐derived material may not reflect their abundance under more physiological conditions.
Differential Effects of Direct and Indirectly Acting Cholinergic Agonists on Growth Hormone Release in Man, and Lack of Effect on Cortisol Secretion
Authors: Casanueva F. F. , Villanueva L. , Cordido F. , Diaz Y. , Cabranes J. A. , Spiegel R. , Dieguez C. 
Published: September 2006

AbstractAcetylcholine plays a key role in the modulation of growth hormone secretion. In fact, growth hormone release after provocative stimuli is blocked by muscarinic cholinergic antagonists, and conversely, indirect cholinergic agonists potentiate growth hormone secretion. To further understand the mechanism by which cholinergic pathways exert their effects, we have compared the growth hormone and cortisol secretion elicited on normal volunteers by pyridostigmine and by RS‐86 (2‐ethyl‐8‐methyl‐2,8‐diazaspiro‐((4,5))‐decan‐1,3‐dion hydrobromide). The former acts by inhibiting acetylcholinesterase, thus being an indirect muscarinic agonist, while the latter is a muscarinic receptor agonist which binds directly to and stimulates cholinergic receptors.In six subjects, pyridostigmine (120 mg po) induced an increase of growth hormone of 11.0±2.4 μg/L at 90 min, significantly greater than following placebo administration (1.4 ± 0.3 μg/L). In another group of five volunteers, RS‐86 was administered in separate tests at a dose of 0.5, 1 and 2 mg po. Growth hormone levels were not altered by any RS‐86 dose compared with placebo values. Neither pyridostigmine nor RS‐86 altered cortisol values.These results suggest that the mechanism of action of the cholinergic agonists is of great importance for their growth hormone‐releasing capabilities, and question the accepted view of a cholinergic regulation of cortisol secretion in man.
Hormonal Activation of Female Sexual Behavior is Accompanied by Hypothalamic Norepinephrine Release
Authors: Vathy Ilona , Etgen Anne M. 
Published: September 2006

AbstractThe present study employed the intracranial microdialysis technique to measure norepinephrine release in the ventrolateral dendritic fields of the ventromedial hypothalamus of freely‐moving animals before and during ovarian steroid (estradiol and progesterone) activation of female sexual behavior (lordosis). One day after implantation of a dialysis probe, animals were injected with 3 μg of estradiol benzoate followed 44 h later by 200 μg of progesterone. Introduction of a male rat 4 h after progesterone treatment was correlated with dramatic increases in extracellular norepinephrine levels measured in dialysates of the ventrolateral ventromedial hypothalamus of female rats which displayed high levels of lordosis behavior. In contrast, female rats given the same steroid treatment but which did not show lordosis responses did not have elevated norepinephrine levels in their dialysates. Moreover, animals that received an estrogen antagonist concurrently with the estrogen treatment had neither an increase in ventromedial hypothalamic levels of norepinephrine during behavior testing nor did they display lordosis. These results indicate a close relationship among ovarian steroids, noradrenergic transmission in the ventromedial hypothalamus, and the expression of female sexual behavior.
Role of the Hypothalamic Paraventricular Nucleus in Mediating Stress‐Related Litter Deficits in the Golden Hamster
Authors: Pratt N. C. , Lisk R. D. 
Published: September 2006

AbstractPrimiparous female hamsters (Mesocricetus auratus) were mated to proven breeders and stressed during early pregnancy. Females were housed singly throughout gestation except for Days 4, 5 and 6 when they were paired for ten‐min intervals three times each day with another female matched for age, weight and day of pregnancy. Within each of the pairs, one female was consistently dominant to the other. Controls were exposed to a novel area instead of a conspecific. At parturition, all pups were counted, sexed and weighed. There were no significant differences between control and dominant females' litter sizes or sex ratios (defined as percentage male). Subordinate females produced significantly smaller litters than control or dominant dams and significantly lower sex ratios than control dams. Subordinates produced fewer males than control or dominant dams, but there were no differences in the number of females produced. The paraventricular nucleus (PVN) of the hypothalamus has been implicated as a relay center for the physiological response to stress. Bilateral lesions of the PVN were performed on another group of females and the same protocol described above was followed after the females recovered from surgery. When this ‘stress relay center’ was lesioned, subordinates did not show the significant deficits in litter size and sex ratio. Sham‐operated females showed a similar response to social stress to that of intact females. These results suggest that subordinate dams produce smaller litters via selective resorption of males in utero and that the PVN may be a relay center for the mediation of this response.
An Electron Microscopic Immunocytochemical Study on the Tyrosine Hydroxylase‐Positive, Dopamine Beta‐Hydroxylase‐Negative Cells in the Pineal Gland of Golden Hamsters
Authors: Shiotani Yahe , Jin Kui Long , Kawai Yuriko , Kiyama Hiroshi 
Published: September 2006

AbstractWe have examined the ultrastructure of tyrosine hydroxylase‐positive, dopamine β‐hydroxylase‐negative neuron‐like cells in the pineal gland of golden hamsters by electron microscopic immunocytochemistry using antiserum to tyrosine hydroxylase. The tyrosine hydroxylase‐positive cells were scattered throughout the parenchyma of the pineal gland. Their cell bodies were oval or spindle‐shaped (maximum diameter 15 to 20 μm) with one or two short cell processes and a large round nucleus. They contained mitochondria, short rough‐surfaced endoplasmic reticulum, Golgi apparatus, and granulated vesicles (50 to 100 nm). The cell membrane was in close contact with the pinealocyte cell body, pinealocyte processes and tyrosine hydroxylase‐negative or ‐positive nerve terminals.
Effect of Tunicamycin, Swainsonine, Castanospermine, Beta‐Hydroxynorvaline and Monensin on the Post‐Translational Processing of Rat Prolactin Molecular Forms
Authors: Bollengier F. , Velkeniers B. , Mahler A. , Vanhaelst L. , Hooghe‐Peters E. 
Published: September 2006

AbstractProlactin cells derived from the anterior pituitaries of female rats were cultured in the presence of tunicamycin, swainsonine, castanospermine, β‐hydroxynorvaline and monensin in order to study their effect on the post‐translational processing of the Mr 17,000, 23,000 and 26,000 prolactin molecular forms. Sodium‐dodecyl‐sulphate polyacrylamide electrophoresis and subsequent immunoblotting revealed that: 1) tunicamycin, swainsonine and castanospermine, compounds that are essentially known as inhibitors of the N‐glycosylation processus, had no effect on Mr 17,000, 23,000 and 26,000 rat prolactin; 2) βhydroxynorvaline, which has been assumed to inhibit processing of pre‐prolactin to mature 23,000 prolactin, did not increase the synthesis of 26,000 rat prolactin. In case of inhibition of the processing of a pre‐prolactin to mature prolactin, one would expect an increase of the pre‐prolactin; consequently, we could not establish the 26,000 rat prolactin, we revealed in immunoblotting, as a pre‐prolactin; 3) monensin affected the post‐translational processing of 17,000 and 26,000 rat prolactin, but left the 23,000 mature form intact. This is an important finding for the following reasons: monensin blocks the transport of secretory and membrane proteins, and this blockade prevents the cleavage of these molecules; indeed, production of 17,000 rat prolactin, a form of cleaved prolactin, was inhibited. Monensin also affects glycosylation and 26,000 rat prolactin has been identified as a presumably O‐iinked glycosylated variant. The fact that its synthesis is inhibited by monensin treatment, but not by inhibitors of the N‐linked process, particularly tunicamycin, and that 26,000 rat prolactin is susceptible to mild alkali and decomposition via β‐elimination are decisive arguments in favour of the O‐linked glycosidic linkage.
Development and Validation of a Two‐Site Immunochemiluminometric Assay for Rat Growth Hormone‐Releasing Hormone
Authors: Page M. D. , Lewis M. D. , Lewis B. M. , Weeks I. , Scanion M. F. 
Published: September 2006

AbstractWe describe the development and validation of a two‐site immunochemiluminometric assay for rat growth hormone‐releasing hormone (GHRH) based on the affinity purification of polyclonal rabbit antisera to rat GHRH using a human 1–29 GHRH affinity column. Assay sensitivity is 3.2 pg/ml using 100 μl of unextracted sample and the working range for the assay within 15% confidence limits is 64 to 5,000 pg/ml. Rat hypothalamic extract and secreted material demonstrated a single large peak of immunoreactive material coeluting with synthetic rat GHRH on high‐performance liquid chromatography with a smaller, earlier peak which probably represents methionine sulphoxide [Met(O)27] GHRH. Extracted material diluted in parallel to the standard curve. Incubated rat hypothalami readily released measurable amounts of rat GHRH which responded appropriately to depolarization with 60 mM K+ in a Ca2+‐dependent manner.
Glucocorticoid Receptor Immunoreactivity in the Rat Intermediate Lobe
Authors: Bertini Luca T. , Westphal Marines M. , de Kloet Ronald E. , Kiss Jozsef Z. 
Published: September 2006

AbstractCells containing Type II glucocorticoid receptor (GR) immunoreactivity were identified in the rat pituitary gland by immunocytochemistry using a specific monoclonal antibody. At light microscopic level, GR immunoreactive cells were located in the intermediate lobe in addition to the well known GR‐containing cell population in the anterior lobe. In both groups of cells GR appeared predominantly in the cell nuclei. Adrenalectomy resulted in a decrease in staining intensity of the anterior lobe and changed the pattern of fluorescence in a minority of cells where cytoplasmic staining became predominant. These changes appeared less marked in the intermediate lobe. Dexamethasone administration reversed the adrenalectomy‐induced alterations of GR staining in both lobes. At the electron microscopic level, GR immunoreactive sites were revealed by the protein A‐gold technique. In contrast to the distribution of fluorescence, GR was localized in cell nuclei as well as in the cytoplasm in both lobes. Quantitative estimates indicate that about 40% more immunoreactive sites are present in the anterior lobe than in the intermediate lobe. The presence of GR in the intermediate lobe suggests that this pituitary region, like the anterior lobe, is influenced by glucocorticoid hormones.
Embryonal Development of Arginine Vasotocin/Mesotocin Gene Expression in the Chicken Brain
Authors: Milewski N. , Lvell R. , Grossmann R. , Ellendorff F. 
Published: September 2006

AbstractAn ontogenic series of chick embryo brains (4, 6, 9,12,14,16 and 18 days of incubation, hatching day: 21) was coronally or saggitally sectioned and investigated for expression of the arginine vasotocin (AVT)/mesotocin (MT) gene. To this end a 39mer oligonucleotide recognizing the AVT/MT encoding sequence of their respective mRNAs was constructed employing optimized codon usage and was used for in situ hybridization. AVT/MT mRNA‐expressing neurons were first detected on embryonal day (E) 6 adjacent to the third ventricle. By E9 the periventricular nucleus had expanded in size but the hybridization signal was weaker. These results suggest a migration of cells in all directions away from the third ventricle into the diencephalon; some perikarya were even observed at the lateral pial surface above the optic chiasm. By E12, brain differentiation had advanced to distinct hypothalamo‐neurohypophyseal nuclei (supraoptic and paraventricular nuclei) as well as to accessory groups expressing AVT/MT mRNA. Two cell types were then distinguishable in the paraventricular nucleus; the specific mRNA was expressed either as a weak or a strong hybridization signal. Comparison with other studies suggested that differentiation had almost attained adult level though cell growth and differentiation of supraoptic and paraventricular nuclei still occurred. This was complete by E18 when individual cells were larger and the intensity of the hybridization signal became very strong.RNase pretreatment depressed the signal by 100%. Northern blot hybridization of RNA extracted from newly hatched chicks verified the specificity of the probe. A single band was evident, indicating an mRNA of approximately 700 bases, which is only found in hypothalamus and not in muscle, liver or extra‐hypothalamic brain, and corresponds in size closely with mammalian vasopressin mRNA.The data demonstrate a very early development (E6) of neurohypophyseal hormone gene expression in the chick embryo brain with important differentiation around E9. At E12 magnocellular neuronal arrangement resembled adult neurons but the gene expression signal increased in intensity until E18.
Cardiovascular Instability Induced by Intracerebroventricular Administration of Vasopressin or Corticotrophin‐Releasing Factor in Conscious Long Evans and Brattleboro Rats
Authors: Gardiner S. M. , Compton A. M. , Bennett T. 
Published: September 2006

AbstractConscious Long Evans and Brattleboro rats, chronically instrumented with pulsed Doppler probes around left renal and superior mesenteric arteries and the distal abdominal aorta, had vasopressin or corticotrophin‐releasing factor administered intracerebroventricularly. In Long Evans rats, vasopressin caused no cardiovascular instability, but in Brattleboro rats, vasopressin caused the development of marked oscillations in blood pressure and heart rate. Under the latter conditions, falls in blood pressure were accompanied by increases in hindquarter blood flow. Similar oscillations in blood pressure, heart rate and regional haemodynamics were seen in Long Evans and Brattleboro rats given corticotrophin‐releasing factor. These results indicate that centrally‐administered vasopressin and corticotrophin‐releasing factor can have an important influence on the control of regional haemodynamics. In some respects the effects of the peptides resemble the changes seen during the defence reaction.
Mechanism of the Haemotensive Action of Porcine Relaxin in Anaesthetized Rats
Authors: Parry L. J. , Poterski R. S. , Summerlee A. J. S. , Jones S. A. 
Published: September 2006

AbstractExperiments were done to examine the pressor effect of iv porcine relaxin in anaesthetized rats. Acute injections of relaxin caused consistent and sustained rises in systemic blood pressure that were dose‐dependent within the physiological range. Pretreatment of rats with a specific vasopressin (V1) receptor antagonist, but not an α‐adrenoreceptor antagonist, substantially reduced the pressor effect of relaxin. After the vasopressin receptor antagonist, small rises in blood pressure occurred after a longer latent period, compared with the responses in intact animals. The data clearly indicate that acute injections of relaxin cause a pressor response that is predominantly affected via the release of vasopressin. The possible sources of the persistent hypertensive component are discussed and it is suggested that relaxin might act through the central angiotensinergic systems to release vasopressin and cause a pressor response.
Effect of Hypothalamic Deafferentation on the Pulsatile Secretion of Luteinizing Hormone in Ovariectomized Lactating Rats*
Authors: Tsukamura Hiroko , Maeda Kei‐ichiro , Ohkura Satoshi , Yokoyama Akira 
Published: September 2006

AbstractThe pulsatile luteinizing hormone (LH) secretion in ovariectomized lactating rats bearing complete (CD), anterior (AD), anterolateral (ALD), posterior (PD), or roof (RD) deafferentation of the hypothalamus was determined. All lactating rats were ovariectomized on Day 2 of lactation (Day 0, day of parturition). The deafferentation of nerve fibres to the mediobasal hypothalamus was performed on Day 6 or 7 of lactation. Twenty‐four h after the surgery, blood samples were taken through the indwelling atrial catheter every 6 min for 3 h. Plasma concentrations of LH and prolactin (PRL) were measured by radioimmunoassay. The loss of LH pulses associated with lactation was still apparent following AD, PD and sham‐deafferentation (SD); pulsatile LH secretion was, however, present in rats with CD, ALD and RD despite continued suckling. The only significant difference in plasma PRL concentrations among the various groups was a reduction in the PRL level in rats with RD in comparison to those with SD. We conclude that the neural signal responsible for the inhibition of pulsatile LH release by suckling is conveyed through the dorsal part of the hypothalamus and PRL does not mediate the suppression of LH pulses in mid‐lactation.