bluuebunny/crossref_metadata_2025_split huggingface dataset:
Glucocorticoids, but not Dopamine, Negatively Regulate the Melanotrophic Activity of the Rabbit Pituitary Intermediate Lobe
Authors: Schimchowitsch Sarah , Plante Martin , Kienlen Pascal , Félix Jean‐Marc , Koch Bernard , Stoeckel Marie‐Elisabeth 
Published: September 2006

AbstractThe leporidae (rabbit and hare)pituitary intermediate lobe(IL)differs from that of other mammals by its neuroendocrine regulation. In particular, it is not submitted to the classic dopaminergic inhibitory control, which has been considered as a repressive factor for the expressionof glucocorticoid receptors (GR) in the mammalian IL. Hence, the present experiments aimed at examining the rabbit IL for the possible existence of GR. Using both immunocytochemistry and binding studies with (3H)‐dexamethasone, we localized GR in the nuclei of IL cells and showed the presence of saturable and high‐affinity type II receptor sites, with Kd∼3.9nM. Also, exposure of cultured IL cells to 10 nM dexamethasone (DEX) resulted in the blockade of melanocyte‐stimulating hormone(αMSH) secretion stimulated by oxytocin (OT). Importantly, the inhibitory effect was reversed by a 100‐fold excess of the glucocorticoid antagonist RU 38486. This is the first study which clearly demonstrates in a mammalian IL, namely the rabbit, the presence of functional GR, involved in the negative regulation of the melanotrophic activity of this gland.
The Secretion of α40‐MSH from Xenopus Melanotropes Involves Calcium Influx through ω‐Conotoxin‐Sensitive Voltage‐Operated Calcium Channels
Authors: Scheenen Wim J. J. M. , de Koning Harry P. , Jenks Bruce G. , Vaudry Hubert , Roubos Eric W. 
Published: September 2006

AbstractThe secretory activity of endocrine cells largely depends on the concentration of free cytosolic calcium. We have studied the mechanisms that are involved in supplying the calcium necessary for the secretion of α‐melanophore‐stimulating hormone (α‐MSH) from melanotrope cells in the pituitary intermediate lobe of the amphibian Xenopus laevis. Using whole‐cell voltage clamp, high‐voltage activated calcium currents were observed, with a peak current between 0 and +20 mV. Two types of Ca2 +‐currents appeared, depending on the experimental setup. An inactivating current, which was observed after a 10 msec depolarizing prepulse, resembled currents through N‐type channels as it was clearly inhibited by 1 μM ω‐conotoxin. The second type was a non‐inactivating current, which was blocked up to 50% by 1 μM nifedipine, indicating its L‐type nature. Only a small component of this inactivating current could be blocked by ω‐conotoxin. No evidence was found for the presence of transient, low‐voltage activated currents.The spontaneous secretion of α‐MSH from superfused neurointermediate lobes was dependent on extracellular calcium, as low calcium conditions (10−4‐10−8 M) rapidly inhibited this process. Under these conditions, secretion was not affected by depolarizing concentrations of potassium chloride. The calcium ionophore A23187 increased secretion under low calcium conditions, but had no effect on spontaneous α‐MSH release. Treatment with CoCI2, a blocker of calcium channels, strongly inhibited the secretory process. These results suggest that spontaneous α‐MSH release depends on influx of calcium through voltage‐operated calcium channels. Nifedipine did not affect spontaneous secretion from lobes, nor did it affect potassium‐induced α‐MSH secretion from dispersed melanotropes. Also BAY‐K8644, a specific agonist of L‐type channels, did not influence α‐MSH release, neither under normal nor under low calcium conditions. On the other hand, ω‐conotoxin dose‐dependently inhibited α‐MSH release, to a maximum of 65% at a concentration of 5 μM, and inhibited potassiuminduced secretion by 40%. Thapsigargin, an agent that mobilizes calcium ions from intracellular stores, had no effect on spontaneous α‐MSH release under normal or low calcium conditions. From these results it is concluded that the spontaneous release of α‐MSH by melanotropes of X. laevis is effectuated by calcium influx through ω‐conotoxin‐sensitive, voltage‐operated N‐type calcium channels and that mobilization of calcium from intracellular stores does not play a major role in the regulation of this release.
Increased Hypothalamic Somatostatin Expression in Mice Transgenic for Bovine or Human GH
Authors: Hurley David L. , Bartke Andrzej , Wagner Thomas E. , Wee Beth E. F. , Phelps Carol J. 
Published: September 2006

AbstractAcute studies of GH removal by hypophysectomy or GH replacement in adult rats have shown that GH has a positive influence on its hypothalamic inhibitory hormone somatostatin (SRIH). The present study was undertaken to assess the effect of lifelong exposure to elevated GH on the development and differentiation of SRIH‐producing hypothalamic neurons, including comparison of differing GH levels and heterologous species of GH. Expression of somatostatin peptide and mRNA was evaluated using respective immunocytochemistry and in situ hybridization in brains of transgenic mice bearing constructs of either human (hGH) or bovine (bGH) linked to metallothionein (MT) promoter or bGH linked to phosphoenolpyruvate carboxykinase (PEPCK) promoter. Nontransgenic littermates served as controls. All transgenic constructs resulted in high levels of circulating heterologous GH and significantly elevated body weights. Both bGH levels and body weights were higher in PEPCK‐bGH than in MT‐bGH mice; mean weights were not different between MT‐bGH and MT‐hGH mice. Numbers of SRIH‐immunoreactive neurons in the hypophysiotropic periventricular nucleus (PeN) of transgenic mice showed a two‐fold increase (P<0.01) relative to control animals; the number of SRIH‐positive cells in the medial basal hypothalamus (MBH) was comparable for transgenic and control mice. Total SRIH mRNA in situ hybridization intensity also showed a two‐fold increase (P<0.05) in the PeN of all transgenic mice compared with controls, and was not elevated in the MBH. The higher levels of GH produced in PEPCK‐bGH transgenic mice led to greater weight gain, but not to greater SRIH expression than in other GH‐transgenic mice, suggesting that the increased SRIH cell number and mRNA in the PeN of MT‐GH‐transgenic mice may represent a plateau of maximal feedback stimulation. The results indicate that lifelong elevated heterologous GH in mice stimulates hypothalamic SRIH expression markedly. It is not known whether this mechanism is direct or indirect via a mediator of GH such as IGF, but the heterologous GH appears to be specific to these hypophysiotropic neurons.
Increased Cortisol Levels in Aging and Alzheimer's Disease in Postmortem Cerebrospinal Fluid
Authors: Swaab D. F. , Raadsheer F. C. , Endert E. , Hofman M. A. , Kamphorst W. , Ravid R. 
Published: September 2006

AbstractThe hypothalamo‐pituitary‐adrenal (HPA) axis is activated during aging and even more so in dementia. Increased levels of corticosteroids may be neurotoxic. Therefore we have investigated cortisol levels in cerebrospinal fluid (CSF) of Alzheimer patients and controls. Ventricular postmortem CSF was collected from clinically and neuropathologically well‐defined Alzheimer patients (n = 26) and control subjects (n = 21). In the group of Alzheimer patients the mean CSF total cortisol level was 83% higher than that in the controls. In presenile Alzheimer patients (< 65 years of age; n = 13) the CSF‐cortisol level was 5 times higher than that of presenile controls (n = 7). In contrast, senile Alzheimer patients (n = 13) and controls of over 65 years of age (n = 14) did not show a significant difference in CSF‐cortisol levels. The presence or absence of a difference in the cortisol‐CSF levels in, respectively, presenile or senile Alzheimer patients as compared to controls was due to the 3.5‐fold rise of CSF‐cortisol in control subjects over 65 years of age as compared with controls under 65 years of age. The CSF‐cortisol levels in presenile and senile Alzheimer patients were similar. No significant correlation was observed in the Alzheimer patients between age of onset of the dementia and CSF cortisol levels or duration of Alzheimer's disease and CSF cortisol levels.The finding that in senile Alzheimer patients cortisol levels were similar to those of unaffected age‐matched controls does not seem to support the cortisol neurotoxicity hypothesis. On the other hand, it should be noted that postmortem ventricular CSF cortisol levels were found to be 13–16 times higher than lumbar puncture CSF cortisol levels of ambulatory patients. This means that the ventricular CSF levels probably reflect the reaction of the HPA‐axis to the process of dying rather than the basal levels of this system. The exact consequences of elevated HPA‐axis activity for the human brain should be studied in more detail.
Role of Neuropeptide Y in the Regulation of Tyrosine Hydroxylase Messenger Ribonucleic Acid Levels in the Male Rat Arcuate Nucleus as Evaluated by in situ Hybridization
Authors: Hong Min , Li Songyun , Pelletier Georges 
Published: September 2006

AbstractNeuroanatomical data have clearly demonstrated the existence of synaptic contacts between neuropeptide Y (NPY) endings and tuberoinfundibular dopaminergic (TIDA) neurons in the rat arcuate nucleus. In order to determine the influence of NPY in the biosynthesis of dopamine, we have studied the effects of NPY and some NPY analogs on tyrosine hydroxylase (TH) gene expression in TlDA neurons in the male rat. The following peptides: NPY, PYY, [Leu31, Pro34]‐NPY (a Y, receptor agonist) and NPY13–36 (a Y2 receptor agonist) were injected into the left lateral ventricle of adult male rats. All the animals were perfused with 4% paraformaldehyde 4 h after injection. Cryostat sections through the arcuate nucleus were processed for quantitative in situ hybridization. The intracerebroventricular injection of NPY, PYY and [Leu31, Pro34]‐NPY induced an increased of 43, 33 and 42%, respectively, in the number of grains overlying TH neurons. On the other hand, the Y2 receptor agonist NPY13–36 did not influence mRNA levels. These data then strongly suggest that NPY positively regulates the genetic expression of TH in rat TlDA neurons via the Y, NPY receptor subtype.
Similarities and Discrepancies in the Signaling Pathway for Nerve Growth Factor in an Insulin Producing Cell Line and a Neural Crest‐Derived Cell Line
Authors: Tazi Abdelali , Czernichow Paul , Scharfmann Raphael 
Published: September 2006

AbstractLike neuronal cells, insulin producing cells (beta cells) possess nerve growth factor (NGF) binding sites and express mRNA coding for the low‐ and high‐affinity NGF receptors, p75NGFR and Trk‐A respectively. Although the role of NGF on neuronal cells is well documented, its function on beta cells is still unknown. As a first step towards the elucidation of the role of NGF on beta cells, we have characterized both types of NGF receptors on INS‐1 cells, a beta cell line derived from a rat insulinorna and studied some early post‐receptor events by comparing the signaling pathway of NGF in those cells and in PC12 cells, a well characterized NGF‐responsive cell line. By polymerase chain reaction, immunocytochemistry, cross‐linking and Western blot analysis, we clearly demonstrated that Trk‐A and p75NGFR, the two NGF receptors expressed in INS‐1 cells and PC12 cells are similar. Moreover, upon NGF treatment, Trk‐A is phosphorylated on tyrosine residues in both cell types in the same dose‐ and time‐dependent manner. These data clearly demonstrate that the first step of NGF signal transduction is similar in PC12 and INS‐1 cells. Although early responsive genes like NGFI‐A and c‐fos are induced in both cell types upon NGF treatment, the induction of c‐jun expression is restricted to PC12 cells. Furthermore, the expression of late responsive genes, such as vgf and transin, which are induced by NGF in PC12 cells, are not induced in INS‐1 cells. In conclusion, although the initial steps of NGF signal transduction are similar in PC12 and INS‐1 cells, some of the later differ. These dissimilarities could suggest that NGF plays different roles in neuronal and pancreatic beta cells.
Hypothalamic‐Pituitary‐Adrenal Function in Chronic Intermittently Cold‐Stressed Neonatally Handled and Non Handled Rats
Authors: Bhatnagar Seema , Meaney Michael J. 
Published: September 2006

AbstractNeonatally handled (H) animals, as adults, exhibit lower ACTH and corticosterone (B) responses to a number of acute stressors compared to their non‐handled (NH) counterparts. However, little is known about activity within the hypothalamic‐pituitary‐adrenal (HPA) axis of H and NH animals under conditions of chronic stress. We, therefore, examined HPA function in adult H and NH rats exposed to chronic intermittent cold stress (4 h of 4°C cold a day for 21 days; H CHR and NH CHR) and in control H and NH (H CTL and NH CTL) rats. H CTL and NH CTL animals displayed comparable ACTH and B responses to a single, acute exposure to cold. We found that H CHR animals exhibited lower levels of ACTH, but not B, during the 21st exposure to cold (the homotypic stressor) compared to the first exposure to cold in H CTL; however, ACTH and B levels in NH CHR were not different from those in NH CTL. In contrast, NH CHR animals hypersecreted ACTH and B in response to restraint (the novel, heterotypic stressor) compared to NH CTL and both H groups, whereas H CHR and H CTL animals did not differ in their responses to restraint. These endocrine responses were associated with increased basal median eminence levels of both CRH and AVP in H CHR and NH CHR relative to their control groups (with NH CHR exhibiting the highest absolute levels of each secretagogue), and with decreased glucocorticoid receptor densities in septum of both H CHR and NH CHR. In addition, the expected lower glucocorticoid receptor density in hippocampus and frontal cortex of NH rats compared to H rats was observed. We believe that the difference in glucocorticoid receptor density between H and NH animals in the hippocampus and frontal cortex aid the associated differences in secretagogue content in the median eminence are related to the hypersecretion of ACTH and B in the NH CHR relative to the other groups. Furthermore, we hypothesize that an active inhibitory process is involved in the adaptation of HPA responses of H CHR animals to the homotypic stressor, and present a working model of regulation of activity within the CRH/AVP neurons in the PVN.
Stimulation of CRH‐Mediated ACTH Secretion by Central Administration of Neurotensin: Evidence for the Participation of the Paraventricular Nucleus
Authors: Rowe Wayne , Viau Victor , Meaney Michael J. , Quirion Rémi 
Published: September 2006

AbstractCentral administration of neurotensin (NT) stimulates hypothalamic‐pituitary‐adrenal (HPA) activity in freely‐moving rats. Increases in adrenocorticotropin hormone (ACTH) and corticosterone (B) were observed 15 rnin following central NT administration and remained elevated for up to 4 h. Of the two NT fragments tested, NT1–8 and NT8–13 only NT8–13 was found to significantly elevate ACTH and B levels. Moreover, NT8–13 activated the HPA axis with a temporal profile similar to NT1–13, suggesting an interaction with the pharmacologically and molecularly characterized NT receptor.Animals pre‐treated intravenously with the corticotropin‐releasing hormone (CRH) antagonist, α‐helical CRH, showed attenuated plasma ACTH and B responses to central NT administration. This indicates that CRH receptor activation is necessary for the stimulatory effects of NT on HPA function. Bilateral lesions of the paraventricular nucleus (PVN) of the hypothalamus significantly reduced NT‐induced stimulation of ACTH and B release suggesting that the PVN is essential for NT's stirnulatory action. Median eminence content studies indicated that acute central NT administration stimulates CRH, but not arginine vassopressin (AVP), release in animals examined 60 min following NT injection. Taken together, these findings suggest that the stimulatory effects of NT on HPA activity occur via specific NT receptors and that one site of action of NT is likely at the level of the PVN where NT elicits the release of CRH.
Regulation of Estrogen Receptor and Progesterone Receptor Messenger Ribonucleic Acid by Estrogen in the Brain of the Whiptail Lizard (Cnemidophorus uniparens)
Authors: Young Larry J. , Nag Pratip K. , Crews David 
Published: September 2006

AbstractReceptive behavior in females vertebrates is controlled by hormones, principally estrogen, secreted by the ovary. Estrogen influences behavior by interacting with a specific estrogen binding protein, or receptor, located in target cells in certain hypothalamic nuclei. To better understand the molecular mechanisms involved in the control of receptive behavior in whiptail lizards, we investigated the effects of exogenous estrogen on t h e regulation of estrogen receptor and progesterone receptor expression in several regions of the brains of Cnernidophorus uniparens. First we determined a dosage of 17β‐estradiol 3‐benzoate (0.5 μg) which reliably induced receptive behavior in ovariectomized C. uniparens. Then using in situ hybridization, we examined the effects of that dosage on the expression of estrogen receptor and progesterone receptor mRNA in the brain 24 h after injection. Estrogen treatment resulted in a significant up‐regulation of estrogen receptor mRNA expression in the ventromedial nucleus of the hypothalamus and torus semicircularis, down‐regulation of estrogen receptor mRNA expression in the lateral septum, and no change in the periventricular nuclei of the hypothalamus, the periventricular nucleus of the preoptic area, and the dorsal hypothalamus. The same dosage resulted in increased progesterone receptor mRNA expression in the ventromedial nucleus of the hypothalamus and the periventricular nucleus of the preoptic area; no significant changes in progesterone receptor mRNA expression were observed in the periventricular nuclei of the hypothalamus or the torus semicircularis, although the differences in progesterone receptor expression in the torus semicircularis approached statistical significance. The up‐regulation of estrogen receptor gene expression by estrogen in the ventromedial nucleus of the hypothalamus of lizards is opposite to that reported in female rats in which estrogen down‐regulates estrogen receptor expression in the ventromedial nucleus of the hypothalamus. We propose that this may be related to differences in reproductive physiology between vertebrates which have extended follicular phases and prolonged periods of estrus and rats, which have an abbreviated follicular phase and brief periods of estrus.
Nuclear and Cytoplasmic Triiodothyronine‐Binding Sites in Primary Sensory Neurons and Schwann Cells: Radioautographic Study During Development
Authors: Walter I. Barakat , Droz B. 
Published: September 2006

AbstractThe effects of the thyroid hormones on target cells are mediated through nuclear T3 receptors. In the peripheral nervous system, nuclear T3 receptors were previously detected with the monoclonal antibody 283 rnAb in all the primary sensory neurons throughout neuronal life and in peripheral glia at the perinatal period only (Eur. J. Neurosci. 5, 379, 7993). To determine whether these nuclear T3 receptors correspond to functional ones able to bind T3, cryostat sections and in vitro cell cultures of dorsal root ganglion (DRG) or sciatic nerve were incubated with 0.1 nM [1251]‐labeled T3, either alone to visualize the total T3‐binding sites or added with a lo3 fold excess of unlabeled T3 to estimate the part due to the non‐specific T3‐binding. After glutaraldehyde fixation, radioautography showed that the specific T3‐binding sites were largely prevalent. The T3‐binding capacity of peripheral glia in DRG and sciatic nerve was restricted to the perinatal period in vivo and to Schwann cells cultured in vitro. In all the primary sensory neurons, specific T3‐binding sites were disclosed in foetal as well as adult rats. The detection of the T3‐binding sites in the nucleus indicated that the nuclear T3 receptors are functional. Moreover the concomitant presence of both T3‐binding sites and T3 receptors CI isoforms in the perikaryon of DRG neurons infers that: 1) [1251]‐labeied T3 can be retained on the T3‐binding ‘E’ domain of nascent CI, isoform molecules newly‐synthesized on the perikaryal ribosomes; 2) the CI isoforms translocated to the nucleus are modified by posttranslational changes and finally recognized by 2B3 rnAb as nuclear T3 receptor. In conclusion, the radioautographic visualization of the T3‐binding sites in peripheral neurons and glia confirms that the nuclear T3 receptors are functional and contributes to clarify t h e discordant intracellular localization provided by the immunocytochemical detection of nuclear T3 receptors and T3 receptor CI isoforms.
Androgen and Estrogen Effects on Vasopressin Messenger RNA Expression in the Medial Amygdaloid Nucleus in Male and Female Rats
Authors: Wang Zuoxin , De Vries Geert J. 
Published: September 2006

AbstractVasopressin messenger RNA (AVP mRNA) expression in the medial amygdala and bed nucleus of the stria terminalis (BST) is almost completely dependent on gonadal steroids. In the BST, the effects of gonadal steroids on AVP mRNA expression are sexually dimorphic. Males have more cells that express AVP mRNA and more AVP mRNA per cell than females. Here we test whether this is also true for the MA.In gonadectomized rats that were treated with testosterone, males had more cells that were labeled for AVP mRNA than females. However, the labeling per cell did not differ between males and females. To assess contribution of testosterone metabolites to these differences, male and female rats were gonadectomized and implanted with empty tubing, or tubing filled with dihydrotestosterone (DHT), estradiol (E), or E plus DHT (E + DHT). The pattern of steroid effects on AVP mRNA expression in the MA was similar in both sexes. Hardly any labeled cells were found in rats with empty implants or rats treated with DHT. Significantly more labeled cells were found in rats treated with E, and even more cells in rats treated with E + DHT. The number of AVP mRNA‐labeled cells was higher in males than in females for E as well as E + DHT treatment, but the labeling per cell did not differ between sexes. These data suggest that the number of MA cells that can express AVP mRNA is higher in males than in females, but the estrogen and androgen responsiveness of individual AVP mRNA‐expressing cells in the MA does not differ between sexes.