bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vasoactive Intestinal Polypeptide mRNA and Peptide Levels are Decreased in the Anterior Pituitary of the Human Growth Hormone‐Releasing Hormone Transgenic Mouse
Authors: Hyde James F. , Morrison David G. , Drake Karen W. , Moore Joseph P. , Maley Bruce E. 
Published: October 2006

AbstractWe recently reported that galanin gene expression is markedly increased in the hyperplastic anterior pituitary gland of the human growth hormone‐releasing hormone (hGHRH) transgenic mouse. To determine if another pituitary peptide hormone with putative growth‐promoting activity is similarly affected, or if this effect is specific to the peptide galanin, we examined vasoactive intestinal polypeptide (VIP) gene expression in the hypothalamic‐pituitary axis of male hGHRH transgenic and non‐transgenic mice. The objectives were to: 1) assess VIP peptide concentrations, 2) estimate relative differences in VIP mRNA levels, 3) determine the effects of acute treatment with 17(3‐estradiol on VIP peptide and mRNA levels, and 4) quantify the density of immunoreactive VIP pituitary cells by immunohistochemistry. Four to five month old male hGHRH transgenic mice and their non‐transgenic siblings were identified by PCR. Immunoreactive VIP concentrations were decreased by 50% in the anterior pituitary glands of hGHRH transgenic mice as compared to non‐transgenic siblings. In contrast, no differences in immunoreactive VIP concentrations were observed in the hypothalamus or frontal cerebral cortex of transgenic and non‐transgenic mice. Treatment with 17β‐estradiol significantly increased VIP concentrations in the anterior pituitary gland of both transgenic and non‐transgenic mice; however, VIP peptide concentrations in the anterior pituitary glands of hGHRH transgenic mice remained 50% lower. Relative differences in VIP mRNA levels were estimated by RT‐PCR, and were found to be 2.5‐fold higher in the anterior pituitary glands of non‐transgenic mice. In contrast, no differences in VIP mRNA levels in the cerebral cortex were detected between transgenic and non‐transgenic mice. Treatment with 17(3‐estradiol increased VIP mRNA levels in the anterior pituitary, but not in the cerebral cortex. In concert with the changes in VIP peptide and mRNA, the density of immunoreactive VIP pituitary cells was decreased approximately 50% in hGHRH transgenic mice. In conclusion, unlike galanin gene expression, VIP peptide and mRNA levels are significantly decreased in the anterior pituitary gland of hGHRH transgenic mice. Moreover, these changes appear to be tissue‐specific and are likely due, in part, to the decrease in the density of VIP‐containing pituitary cells in the hyperplastic pituitary. Although the pituitary cell type(s) synthesizing VIP remains unclear, these data suggest that VIP in the anterior pituitary is not stimulating pituitary tumor development in hGHRH transgenic mice.
In vivo Microdialysis of the Hypothalamus: a Suitable Method to Study the Function of Hypophysiotropic Neurons in the Rat
Authors: Cattaneo Lorena , Müller Eugenio E. , Cocchi Daniela 
Published: October 2006

AbstractBrain microdialysis is a method commonly exploited by neuropharmacologists to study the mechanism of action and preclinical features of centrally acting drugs. It allows measurement of chemical messengers released into the extracellular space, providing a first approximation of neuronal function in selected areas.In this study we have applied the microdialysis of the hypothalamus to evaluate the release of somatostatin from neurosecretory neurons which are involved in growth hormone regulation and validated this method with different challenges.
Median Preoptic Neurones Projecting to the Supraoptic Nucleus are Sensitive to Haemodynamic Changes as well as to Rise in Plasma Osmolality in Rats
Authors: Aradachi Hiroshi , Honda Kazumasa , Negoro Hideo , Kubota Toshihiko 
Published: October 2006

AbstractExtracellular single unit activity was recorded from 73 neurones in the median preoptic nucleus (MnPO), identified by antidromic activation as projecting to the supraoptic nucleus (SON) area in urethane‐anaesthetized male rats. Thirteen of 73 identified MnPO neurones were silent, and 44 of 60 spontaneously active MnPO neurones were tested for their responses to electrical stimulation of the nucleus tractus solitarius (NTS). The cells were divided into 4 groups according to their responses; those which were excited orthodromically (OD+; n = 15), those which were unresponsive (UN; n = 21), those which were inhibited orthodromically (OD−; n=4), those which showed initial inhibition followed by excitation (OD+ n = 4). Some of these neurones were further tested for their responses to haemorrhage and/or increase in blood pressure produced by intravenous administration of the oe‐agonist, phenylephrine, and/or to hyperosmotic stimulation produced by intraperitoneal injection of 1.5 M NaCl. Six out of 10 OD+ cells were excited by haemorrhage, 6 out of 11 OD+ cells were inhibited by phenylephrine, and 5 out of 9 OD+ cells were excited by hypertonic saline. On the other hand the UN cells tended to be unresponsive to each type of stimulus. Three out of 7 OD+ cells were excited by both haemorrhage and hypertonic saline, and 3 out of 8 OD+ cells were inhibited by phenylephrine and excited by hypertonic saline. The results may suggest that MnPO neurones which receive afferent input from the NTS may be sensitive not only to haemodynamic change but also to change in plasma osmotic pressure and that such population of MnPO neurones may integrate a part of the haemodynamic and osmotic information and contribute to the control of neurohypophysial hormone release.
Ovarian Steroid Regulation of Estrogen and Progesterone Receptor Messenger Ribonucleic Acid in the Anteroventral Periventricular Nucleus of the Rat
Authors: Simerly R. B. , Carr A. M. , Zee M. C. , Lorang D. 
Published: October 2006

AbstractThe anteroventral periventricular nucleus of the preoptic region (AVPV) represents a key site for hormonal feedback on gonadotropin secretion. It plays a critical role in the neural control of luteinizing hormone secretion and contains high densities of neurons that express receptors for estrogen and progesterone. In this study in situ hybridization was used to examine the expression of mRNAs encoding the estrogen (ER) and progesterone (PR) receptors in the AVPV during the estrous cycle. ER gene expression fluctuated during the cycle with the lowest levels of ER mRNA observed in animals killed on the afternoon of proestrus, and the highest levels present in animals killed during metestrus. This apparent inverse relationship between circulating levels of estradiol (E2) and ER mRNA levels in AVPV neurons was supported by the observation that treatment of ovariectomized rats with E2 suppressed expression of ER mRNA in the AVPV. The influence of progesterone (P4) on ER expression was less pronounced, but a significant increase in ER mRNA in the AVPV was detected 3 h after treatment with P4. In contrast, PR mRNA levels were highest in the AVPV during diestrus and lowest on the morning of proestrus suggesting that PR expression in the AVPV is regulated in a complex manner that may reflect the combined regulatory effects of E2 and P4. E2 treatment caused a dramatic induction of PR mRNA in the AVPV, but P4 did not affect PR mRNA expression acutely, although PR mRNA appears to be attenuated in the AVPV 27 h after P4 treatment. These findings suggest that ovarian steroid hormones regulate ER and PR gene expression in the AVPV during the estrous cycle, which may represent molecular events that contribute to cyclic changes in the responsiveness of AVPV neurons to steroid hormones.
Different Effects of Somatostatin on in vitro Growth Hormone Release in Two Porcine Breeds with Different Growth Rates1
Authors: Torronteras Rafael , Gracia‐Navarro F. , Elsaesser Folkmar 
Published: October 2006

AbstractA perifusion system of anterior pituitary (AP) tissue was used to investigate the temporal interaction of growth hormone‐releasing factor (GRF) and somatostatin (SRIF) in the control of GH secretion in two pig breeds, Göttingen Miniature Pig (GMP), a small obese breed, and German Landrace (GLR), a conventional lean breed. AP tissue pieces derived from sexually mature ovariectomized animals were perifused (6 replicates per treatment) and fractions were collected at 10 min intervals. Basal GH release (ng‐mP‐1 mg‐1 AP) in GLR was twice that of GMP (P < 0.001). Exposure to 10 min pulses of 1 nM GRF repeated 3 times at 2 h intervals resulted in rapid stimulatory GH responses (area under the curve) which became attenuated (P < 0.05) over time in GMP but not in GLR. Surprisingly, during and following the exposure of AP tissue from GMP to 10‐, 20‐, or 40‐min pulses of 10 nM SRIF alone, GH release was markedly stimulated (P < 0.05), while AP tissue from GLR only showed a weak rebound GH release after SRIF pulses. With AP tissue from GLR low concentrations (0.1 nM SRIF) amplified GRF‐induced GH release, whereas 1 nM or 10 nM SRIF inhibited GRF‐induced GH release. However, concomitant exposure of AP tissue from GMP to 0.1, 1 or 10 nM SRIF during a GRF pulse markedly enhanced the GH response (P < 0.05), compared to 1 nM GRF alone, except for 1 nM SRIF which inhibited the GH response to the first GRF pulse. Thus the presence of SRIF, and not only its withdrawal, is an important factor in setting the timing and duration of GH pulses in both breeds. In GLR the concentration of SRIF is more important than the duration and/or type of SRIF pulse. In contrast, in GMP type and/or duration of SRIF pulses seem to be crucial to optimize pulsatile GH release and even determine peak height of GH pulses caused by GRF. These findings indicate clear breed differences in the role of SRIF and in the control of GH release by the interplay of GRF and SRIF. The ‘paradoxical’ effect of SRIF suggests that the role of SRIF is much more complex than that of a mere inhibitor and whose real role could be a modulator either of GH pulse and/or GRF action on GH release.
Changing Effect of i.c.v. IL‐1β on Vasopressin Release in Anaesthetized, Female Rats at Different Stages of Lactation: Role of Prostaglandins and Noradrenaline
Authors: Wilson Brian C. , Fulop Kathleen , Summerlee Alastair J. S. 
Published: October 2006

Abstractlnterleukin‐1β stimulates oxytocin and vasopressin release in conscious, male rats and causes a rise in blood pressure. These experiments were done to: A) examine the effect of i.c.v. interieukin‐1 β (1 ng/μl) on circulating levels of vasopressin in female rats at different stages of lactation and B) determine if α‐adrenergic mechanisms and/or prostaglandins were involved as mediators. Urethane‐anaesthetized non‐lactating rats and rats at Day 7, 10, 20 and 26 of lactation were set up for arterial blood sampling and i.c.v. injections. One mL blood samples were obtained in one min periods before, and at 1, 2.5, 5, 10, 30, 60 and 120 min after the following treatments: i.c.v. treatment with either interleukin‐1β (1 ng in 1 μl PBS‐BSA) or PBS‐BSA (1 μl) as a vehicle control; or i.c.v. treatment with interleukin‐1β following pretreatment with either phentolamine (1.7 ng/μl i.c.v.) or indomethacin (1 ng/μl i.c.v.). As blood was sampled, isotonic saline was infused (1 mL per min) and blood pressure was monitored to minimize any hypovolemic effects due to sampling. Extracted plasma was assayed using a specific vasopressin radioimmunoassay, lnterleukin‐1 β i.c.v. stimulated the release of vasopressin above that elicited by PBS‐BSA alone in non‐lactating rats resulting in an approximate 1.2 to 2‐fold increase in plasma hormone levels. Throughout the first half of lactation, vasopressin responsiveness to i.c.v. interleukin‐1β treatment was markedly attenuated. In latter stages of lactation, the response recovered and resembled that of non‐lactators around the time of weaning. Prostaglandins consistently mediate a stimulatory action of interleukin‐1β on vasopressin release whereas α‐adrenergic mechanisms mediate a depression of interleukin‐1β‐induced vasopressin release during the early to middle stages of lactation. It is possible that the depression in interleukin‐1β‐stimulation of vasopressin release in early to mid‐lactation is conducive for nursing to occur and that the increase in vasopressin responsiveness towards the latter stages of lactation represents a component of the weaning process.
A Subset of Estrogen Receptor‐Containing Neurons Project to the Median Eminence in the Ewe
Authors: Jansen Heiko T. , Hileman Stanley M. , Lubbers Laura S. , Jackson Gary L. , Lehman Michael N. 
Published: October 2006

AbstractThe neural pathways responsible for conveying the steroid feedback signals that ultimately affect reproductive neuroendocrine function remain largely undefined. One possibility involves a direct projection from estrogen receptor (ER)‐containing neurons to the median eminence (ME), a site of neuroendocrine peptide release. To examine this possibility, 8 ewes received stereotaxic injections of the retrograde neuronal tract‐tracing compound cholera toxin‐β subunit (CTβ) into the ME. Neurons sending projections to the ME and containing ER were identified using a dual‐label immunoperoxidase method. Double‐labeled cells were found in distinct regions: (1) the ER‐rich arcuate nucleus (ARC) that contained the greatest number of double‐labeled cells, and (2) the organum vasculosum of the lamina terminalis (OVLT) which contained a very consistent, but low, number of double‐labeled cells. While a fairly large number of retrogradely‐labeled ARC neurons containing ER were identified, the majority of ER‐containing ARC neurons were unlabeled and thus send projections elsewhere. Other regions containing high concentrations of ER‐positive cells such as the medial preoptic area (MPOA), anterior hypothalamic area, and ventrolateral portion of the ventromedial hypothalamic nucleus, were devoid of double‐labeled cells. Similarly, regions rich in neuroendocrine neurons such as the periventricular hypothalamus and paraventricular and supraoptic hypothalamic nuclei contained no double‐labeled cells. These results suggest that modulation of neuroendocrine secretory activity may occur directly at the level of the ME by ER‐containing neurons located within restricted regions of the hypothalamus and forebrain. However, the relatively low proportion of ER‐containing neurons projecting to the ME suggests that the influence of estradiol upon neuroendocrine function also may include target sites other than the ME.
Adenosine Inhibits L‐ and N‐Type Calcium Channels in Pituitary Melanotrophs. Evidence for the Involvement of a G Protein in Calcium Channel Gating
Authors: Mei Yan Ai , Le Foll Frank , Vaudry Hubert , Cazin Lionel 
Published: October 2006

AbstractIt has been previously demonstrated that activation of A1 adenosine receptors in frog melanotrophs causes inhibition of spontaneous action potential discharges and alpha‐melanocyte‐stimulating hormone secretion. In the present study, we have investigated the effect of adenosine on high‐voltage‐activated (HVA) calcium currents in cultured melanotrophs, using the whole‐cell variant of the patch‐clamp technique with barium as a charge carrier. Adenosine and the specific A1 adenosine receptor agonist R‐PIA (50 μM each) produced a decrease of the amplitude of the barium current, while the selective A2 adenosine receptor agonist CGS 21680 did not affect the current. The inhibitory effect of R‐PIA was observed throughout the activation range of the current, with stronger responses at more positive potentials. R‐PIA inhibited both the L‐ and N‐type components of the current, the effect on the N‐component being two‐fold higher than on the L‐component. The inhibitory effect of R‐PIA was rendered irreversible by addition of GTPyS (100 μM) to the intracellular solution. Pre‐treatment of the cells with pertussis toxin (1 μg/ml; 12 h) totally abolished the effect of R‐PIA on the HVA calcium channels. Conversely, addition of a high concentration of cAMP (100 μM) together with the phosphodiesterase inhibitor IBMX (100 μM) to the intracellular solution did not modify the effect of R‐PIA on the current.It is concluded that, in frog melanotrophs, adenosine induces inhibition of L‐ and N‐calcium currents and that this effect is mediated by a pertussis toxin‐sensitive G protein. Our data also indicate that the inhibitory effect of adenosine on the calcium currents is not mediated by inhibition of adenylyl cyclase.
Evidence for a Trophic Action of the Glycoprotein Hormone α‐Subunit in Rat Pituitary
Authors: Van Bael Annemie , Denef Carl 
Published: October 2006

AbstractThe effect of the α‐subunit of luteinizing hormone (LHα) on lactotroph growth in 14‐day‐old rat pituitary was studied in vitro using a reaggregate pituitary cell culture system. LHα significantly expanded both the total population of cells expressing prolactin mRNA and the number of [3H]thymidine incorporating prolactin mRNA expressing cells. No such effect could be elicited by LH. Both effects were inhibited by simultaneous addition of an anti‐LHα antiserum but not by normal rabbit serum. Anti‐LHα antiserum added alone to the cultures caused a small decrease in the number of prolactin mRNA expressing cells and in [3H]thymidine labelling of the latter. It is concluded that LHα may be a trophic factor of lactotrophs not only during fetal development, as suggested by others previously, but also during the rapid expansion of this cell type during postnatal life in the rat.
Corticosterone Controls lnterleukin‐1β Expression and Sickness Behavior in the Rat
Authors: Pezeshki Gita , Pohl Thomas , Schöbitz Bernd 
Published: October 2006

AbstractWe studied the effect of corticosterone on interleukin (IL)‐1β synthesis, body temperature, general activity, food consumption and fluid intake in rats treated with bacterial lipopolysaccharide (LPS). Radiotelemetry was used to assess body temperature and locomotor activity in combination with continuous automated recordings of feeding and drinking. This technique was developed as a novel method to identify and measure sickness behavior in rodents. The animals were (a) sham‐operated, (b) adrenalectomized or (c) sham‐operated and treated with corticosterone (10 mg/kg, subcutaneously). They were then intraperitoneally injected with vehicle or LPS at a dose (100 μg/kg) that in sham‐operated rats induced fever and anorexia, reduced spontaneous activity and increased IL1‐β mRNA in spleen and adrenals as determined by Northern blot analysis. Adrenalectomized rats produced larger amounts of splenic IL‐1β mRNA, reduced their general activity much more and developed a mild adipsia as compared with adrenal‐intact animals. Administration of corticosterone 1 h before LPS lowered the splenic IL‐1β mRNA content compared to LPS‐treated adrenal‐intact rats that did not receive corticosterone and inhibited fever and anorexia, whereas the glucocorticoid did not attenuate the endotoxin‐induced suppression of locomotor activity. Our data suggest that during inflammatory conditions body temperature, sickness behavior and the synthesis of IL‐1β are controlled by corticosterone. Different components of sickness behavior seem to be independently regulated and are under differential control by glucocorticoids.
Facilitatory Effects of Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) on Neurons in the Magnocellular Portion of the Rat Hypothalamic Paraventricular Nucleus (PVN) in vitro
Authors: Uchimura Daisuke , Katafuchi Toshihiko , Hori Tetsuro , Yanaihara Noboru 
Published: October 2006

AbstractTo establish the role of pituitary adenylate cyclase activating polypeptide (PACAP), a member of vasoactive intestinal polypeptide (VIP) family, as a neurotransmitter/neuromodulator in the central nervous system, the effects of PACAP38, PACAP27 and VIP on the single neuron activity in the magnocellular portion of the hypothalamic paraventricular nucleus (mg.PVN) were examined in rat brain slice preparations. Extracellular recordings were made from 111 neurons in the mg.PVN, which fired spontaneously at an average rate of 1.85 ± 0.2 spikes/s (mean ± SEM). PACAP38 and PACAP27 were applied to 78 and 33 of the 111 neurons, respectively. Perfusion with PACAP38 in doses between 10 nM and 1 μM increased the firing rate of 56 (71.8%) of the 78 neurons in a dose‐dependent manner. The threshold dose of PACAP38 to excite the neurons seemed to lie below 10 nM. The application of PACAP27 (1 μM) also increased the firing rate of 19 (57.6%) of the 33 neurons tested. Eleven (52.4%) of 21 neurons which were excited by PACAP38 also showed excitation following perfusion with VIP (1 μM). The responses to PACAP38 in 12 of 20 neurons and those to VIP in 6 of 9 neurons tested were still observed in a low Ca2+ and high Mg2+ medium. Although there was no difference in the mean latency between the responses to PACAP38 (1 μM) and VIP (1μM) (2.1 ± 0.1 min and 2.4 ± 0.4 min, respectively), the duration of the PACAP38‐induced excitation (59.0 ± 5.0 min) was much longer than that of the VIP‐induced one (18.8 ± 3.1 min). The PACAP38 (30 nM)‐induced excitation was reversibly blocked by a concurrent application of PACAP5‐38 (300 nM), a PACAP receptor antagonist. While a selective VIP receptor antagonist, [Lys1, Pro2,5, Arg3,4, Tyr6]‐VIP (1μM), did not affect the excitatory responses to PACAP38 (300 nM), it completely blocked the VIP (1μM)‐induced excitation. These findings suggest that PACAP may therefore modulate the secretion of the pituitary hormones at least partly by its action on the neurons in the mg.PVN through the activation of specific receptors for PACAP.
Prostaglandin Fever in Rats Throughout the Estrous Cycle Late Pregnancy and Post Parturition
Authors: Martin Sheilagh M. , Malkinson Terrance J. , Veale Warren L. , Pittman Quentin J. 
Published: October 2006

AbstractWe have examined the influence of natural variations in endocrine status on the ability to generate a prostaglandin‐induced fever in virgin female, pregnant and lactating rats and compared responses to those in male rats. Endocrine status of virgin female rats was assessed from examination of vaginal smears and time of parturition noted to enable accurate dating of pre‐ and postparturient fevers. Unanesthetized rats, previously prepared with intraventricular guide cannulas and intraperitoneal telemetry thermistors, were given intraventricular injections of prostaglandin E, (2–100 ng/5 μl) and temperatures monitored for 3 h after injection. Virgin females developed significantly larger fevers than did males at higher doses. There were no significant alterations in either fever height or duration as a function of the phase of the reproductive cycle in the females. Both pregnant and postparturient rats within the several days around birth displayed significantly lower fevers than did virgin females, but there was no further reduction in the immediate periparturient period. These data indicate that there are sex‐, and possibly hormone‐dependent differences in the central mechanisms involved in fever generation and antipyresis.