bluuebunny/crossref_metadata_2025_split huggingface dataset:
Arginine Vasopressin‐lnduced Sensitization in Brain: Facilitated Inositol Phosphate Production Without Changes in Receptor Number
Authors: Poulin Paule , Pittman Quentin J. 
Published: September 2006

AbstractArginine vasopressin (AVP) has been shown to have a unique sensitization effect whereby repeated injection of AVP into a lateral cerebral ventricle or a mediobasal region of the rat forebrain below the lateral septum and including the anterior hypothalamus referred to as the ventral septal area, causes enhanced motor responses to the ligand. To elucidate possible neuronal mechanisms responsible for AVP sensitization, 1) we determined the dose and the time required for the development and expression of AVP sensitization, and 2) we tested the hypotheses that AVP sensitization may result in a) alteration of septal AVP V1 receptor affinity or number, and/or b) alteration of septal AVP V1 receptor signal transduction (phosphatidylinositol hydrolysis) mechanisms. Our behavioral data show that the magnitude of AVP sensitization varies with dose and time, and the effect is dependent on the time interval between injections, in that an initial intracerebroventricular AVP injection enhances the sensitivity of the animals to the motor effects of similar AVP injections given 6 h to 6 days later but not to injections given hourly or weekly. No changes in septal AVP binding site density and affinity, as measured by [3H]AVP binding to septal synaptic plasma membrane, were found in sensitized animals; [3H]inositol monophosphate stimulation in response to AVP in septal slices, however, was found to be significantly enhanced. This enhanced [3>H]inositol monophosphate stimulation appears specific to a V1‐type receptor because it was significantly reduced in the presence of the V1 receptor antagonist, d(CH2)5Tyr(Me)AVP, and was not found using oxytocin or the V2 receptor agonist, DDAVP. Our results therefore indicate that receptor binding, while critical to peptide neurotransmitter action, is not the sole factor for determining responsiveness. Rather, an appropriate schedule of AVP administration, which may cause changes in postreceptor effector system(s) such as inositol phosphate hydrolysis, appears most important.
Effects of Lipocortin 1 and Dexamethasone on the Secretion of Corticotrophin‐Releasing Factors in the Rat: in vitro and in vivo Studies
Authors: Loxley H. D. , Cowell A‐M. , Flower R. J. , Buckingham J. C. 
Published: September 2006

AbstractLipocortin 1 (LC1: also called annexin 1) was first described as a putative second messenger protein for the anti‐inflammatory steroids in peripheral tissues. In the present study, in vitro and in vivo methods were used to examine its potential role within the hypothalamus as a mediator of the regulatory actions of the glucocorticoids on the hypothalamo‐pituitary‐adrenocortical axis of the rat.In the in vitro studies, the effects of human recombinant LC1 (hu‐r‐LC1) on the concomitant release of the two major corticotrophin‐releasing factors (CRF‐41 and arginine vasopressin, AVP) from isolated hypothalami removed from chronically adrenalectomized rats were compared with those of dexamethasone in the presence and absence of appropriate secretagogues, namely phospholipase A2 (PLA2), interleukin‐6 (IL‐6) and a non‐specific depolarizing agent, K+ (56 mM). The spontaneous release of CRF‐41 in vitro was unaffected by either hu‐r‐LC1 (5 to 100 ng/ml) or dexamethasone (1 μM). Both compounds however reduced the release of the neuropeptide evoked by IL‐6 (5 ng/ml) but failed to modify the secretory responses to PLA2 (25 U/ml) or K+ (56 mM). Dexamethasone (1 μM) had no effect on the basal release of AVP but effectively blocked the secretion of the peptide induced by either IL‐6 (10 ng/ml) or PLA2 (25 U/ml). In complete contrast, hu‐r‐LC1 (5 to 100 ng/ml) stimulated the release of AVP and potentiated the secretory responses to IL‐6 (10 ng/ml) and PLA2 (25 U/ml) but not to K+ (56 mM). The hypothalamic responses to PLA2 stimulation (25 U/ml) were associated with significant (P<0.01) increases in prostaglandin E2 release which, in some instances, were potentiated by hu‐r‐LC1 (5 to 20 ng/ml). In vivo, administration of histamine (0.6 mg/100 g body wt, ip) produced significant (P<0.01) increases in the serum corticosterone concentration and in the hypothalamic LC1 content. Neither hu‐r‐LC1 (0.6 to 1.2 μg) nor a polyclonal anti‐LC1 antibody (3 μl, diluted 1:200), injected intracerebroventricularly (icv), influenced either the resting serum corticosterone concentration or the hypersecretion of the steroid evoked by histamine stress. A lower dose of the recombinant protein (0.3 μg icv) also failed to alter basal corticosterone release but, in contrast to the higher doses, potentiated the pituitary‐adrenocortical responses to histamine.The results suggest that LC1 may contribute to some aspects of peptide release in the hypothalamus but that its actions are not necessarily related to those of the glucocorticoids.
Hormonal Control of Sex Differences in the Brain, Behavior and Accessory Sex Structures of Whiptail Lizards (Cnemidophorus Species)
Authors: Wade Juli , Huang Junn‐Ming , Crewst David 
Published: September 2006

AbstractThe effects of steroid hormones on sexual dimorphisms in the brain, behavior and accessory sex structures were investigated in two species of whiptail lizards. The studies were conducted both in adults and hatchlings of a sexually reproducing species (Cnemidophorus inornatus) and an all‐female species (C. uniparens) which displays ‘sexual’ behaviors typical of males and females. Adults were gonadectomized and approximately 3 months later given either a Silastic capsule filled with sex steroid or an empty capsule. Young animals of both species were left intact and given a capsule on the day of hatching. An additional group of C. uniparens was ovariectomized on the day of hatching. Following treatment, measures of oviduct (estrogen‐dependent), renal sex segment (androgen‐dependent) and wolffian duct (androgen‐dependent) hypertrophy were taken in some experiments. Animals were also tested for sexual behavior in some of the studies. The volumes of the anterior hypothalamus‐preoptic area and ventromedial hypothalamus were measured in each individual. Estrogen, testosterone and dihydrotestosterone stimulated peripheral structures at both time periods in both sexes and species. The hormones also stimulated courtship and copulatory behaviors in many of the adult animals. However, testosterone in the anterior hypothalamus‐preoptic area of male C. inornatus was the only treatment which produced parallel effects on the volume of a brain area and the behaviors which it controls. These data add whiptail lizards to the list of species in which steroid hormones affect the volume of brain regions in adulthood, but suggest that such changes in morphology are not necessarily predictive of functional differences.
Is Vasopressin Preferentially Released from Corticotropin‐Releasing Factor and Vasopressin Containing Nerve Terminals in the Median Eminence of Adrenalectomized Rats?
Authors: de Goeij Dimphena C. E. , Berkenbosch Frank , Tilders Fred J. H. 
Published: September 2006

AbstractThe effects of adrenalectomy (ADX) on the amounts of immunoreactive corticotropin‐releasing factor (CRFj) and arginine vasopressin (AVPi) that are stored in the zona externa of the median eminence (ZEME) were investigated by means of quantitative immunocytochemistry. Although ADX of male Wistar rats for 1 week or 4 weeks did not affect CRFi in the ZEME as compared to sham‐operated or intact controls, AVPi showed a progressive accumulation. The ratio of AVPi over CRFi in the ZEME had already increased 1 day after ADX. However, it should be noted that the exact changes in CRFi and AVPj as measured by radioimmunoassay and/or quantitative immunocytochemistry were dependent on the substrain of rats used. The secretion rate of CRFi and AVPj was estimated in 1 week and 4 week ADX rats, by measuring the disappearance rate of CRFi and AVPi from the ZEME after blockade of fast axonal transport, by a low non‐toxic dose of colchicine (5 μg per rat). In contrast to intact rats, where this dose of colchicine did not affect CRFi or AVPi in the ZEME, ADX rats showed a progressive depletion of the CRFi and AVPi stores as measured 2.5 and 5 h later. In 1 week ADX rats, CRFi and AVPi both disappeared at a rate of 7% to 8% of their stores per hour. In contrast, after 4 weeks of ADX the fractional disappearance rates of CRFi and AVPi were different and were 3% and 8% of the content per hour, respectively. This indicates that in long‐term ADX rats the chance of AVP being released from the ZEME is more than twice that of CRF. Since most, if not all, of the CRF; containing nerve terminals in the ZEME of ADX rats costore AVP, we hypothesize that in long‐term ADX rats AVP may be preferentially secreted from AVP and CRF costoring nerve terminals.
Altered Ratios of Beta‐Endorphin:Beta‐Lipotropin Released from Anterior Lobe Corticotropes with Increased Secretory Drive.
Authors: Young Elizabeth A. , Day Robert , Schafer Martin , Watson Stanley J. , Akil Huda 
Published: September 2006

AbstractA number of stimuli including acute footshock and electrically‐induced seizures lead to release of β‐endorphin immunoreactivity from the anterior pituitary corticotropes. Gel filtration of this β‐endorphin immunoreactivity indicates that approximately 3‐fold more β‐endorphin than β‐lipotropin is released into plasma following these acute stressors. A similar preponderance of β‐endorphin over β‐lipotropin is seen in the media of short‐term anterior lobe cell suspensions stimulated with ovine corticotropin‐releasing hormone. Previous studies indicated that footshock stress, when administered repeatedly, can increase the biosynthesis of anterior lobe proopiomelanocortin (POMC) as indicated by increased steady state adrenocorticotropin/β‐endorphin content as well as increased POMC mRNA levels and increased POMC biosynthesis and rate of processing as measured by pulse‐labeling and pulse‐chase studies. The goal of the present studies was to determine whether this increased biosynthetic drive results in an alteration in the end products secreted with repeated stress. Acute footshock in a rat which has received 14 days of chronic footshock releases proportionately more β‐lipotropin than is released in a naive rat. Chronic electrically‐induced seizures, which also increase anterior lobe POMC derived peptide stores, lead to a similar shift in the ratio of β‐lipotropin:β‐endorphin released following stress. These data suggest that chronic drive and the subsequent changes in POMC peptide stores may lead to a decrease in the proportion of β‐endorphin size immunoreactivity in the releasable pool of the anterior lobe corticotrope, thus altering the hormonal signal from the anterior lobe corticotrope.
Glucocorticoid Receptor Function in Rat Pituitary Intermediate Lobe is Inhibited by an Endogenous Protein
Authors: Sheppard Karen E. , Autelitano Dominic J. , Roberts James R. , Blum Mariann 
Published: September 2006

AbstractThough glucocorticoids inhibit proopiomelanocortin (POMC) gene expression and POMC‐derived peptide release from corticotroph cells of the anterior pituitary, the regulation of this gene by glucocorticoids is less clear in the melanotroph cell of the pituitary intermediate lobe. To examine the difference between glucocorticoid sensitivity of the anterior lobe (AL) and intermediate lobe (IL) of the pituitary we have examined glucocorticoid receptor (GR) status of these two tissues and the role glucocorticoids play in regulating IL POMC gene expression. The rate of in vivo GR gene transcription, measured by nuclear run‐on assay was consistently higher in the pituitary neurointermediate lobe (NIL) compared with the AL of the same animals. On a concentration basis, cytoplasmic GR mRNA in the NIL was similar to that found in the AL, and GR binding using [3H]dexamethasone (DEX) as ligand demonstrated similar concentrations of specific [3H]DEX binding in acutely isolated AL and NIL tissues. The specific Type II corticosteroid receptor ligand RU28362 displaced [3H]DEX binding to levels equivalent to non‐specific binding, thus indicating that DEX was binding only to Type II corticosteroid receptors. To assess the direct action of glucocorticoids on POMC gene expression, NIL cells were cultured for 7 days and then treated with DEX. One hour DEX treatment of NIL primary cultures had no effect on levels of POMC heteronuclear RNA levels; in contrast, DEX induced a rapid and potent inhibition of POMC heteronuclear RNA levels in cells treated with the protein synthesis inhibitor puromycin. These data suggest that GR is present in the normal IL of the rat pituitary, but that its ability to regulate POMC gene expression is inhibited by the presence of one or more rapidly turned over proteins.
Estradiol Modulates Insulin‐Like Growth Factor I Receptors and Binding Proteins in Neurons from the Hypothalamus
Authors: Pons S. , Torres‐Aleman I. 
Published: September 2006

AbstractTrophic effects of 17β‐estradiol (βE2) on in vitro developing hypothalamic cells have been reported. Insulin‐like growth factor I (IGF‐I) is also a potent trophic factor for cultured hypothalamic cells. An interaction between sexual steroids and insulin‐like growth factors (IGFs) in modulating growth of hypothalamic cells has been suggested. Thus, we tested whether βE2 modulates the levels of IGF‐I, its membrane receptor and its binding proteins in rat hypothalamic culturs. Using both neuron‐ and glial‐enriched cultures obtained from fetal rat hypothalami we found that addition of βE2 elicited a significant increase in IGF‐I receptor levels in neurons, without affecting its affinity. On the other hand, the three different IGF‐binding proteins (IGFBPs) found in the conditioned medium of the cultures were differentially modulated by βE2 in the two types of cells studied. Overall, neuronal cultures produced greater amounts of IGFBPs after treatment with βE2, with IGFBP2 reaching significantly higher levels. On the contrary, treatment with βE2 did not significantly alter the amounts of IGFBPs produced by glial cells. Finally, the levels of immunoreactive IGF‐I found either in the medium or in cellular extracts in both neuronal and glial cultures were not modified by treatment with βE2. These results strongly support previous observations of a trophic synergistic interaction between IGFs and βE2 on hypothalamic cells. Thus, an increase in IGF‐I receptors and/or IGFBPs after exposure to βE2 may result in an enhanced response of hypothalamic neurons to IGF‐I. Further, the present findings strengthen our recent observation that the effects of βE2 on hypothalamic glial cells are neuronally mediated, since IGF‐I receptors and IGFBPs are modulated by this sex hormone in neurons, but not in glial cells.
Arginine Vasotocin Gene Expression and Hormone Synthesis During Ontogeny of the Chicken Embryo and the Newborn Chick
Authors: Mühlbauer E. , Hamannt D. , Xu B. , Ivell R. , Udovic B. , Ellendorff F. , Grossmann R. 
Published: September 2006

AbstractChicken embryos at different developmental stages (embryonal day (E) 6 to 21) and chicks at posthatch day 1 (D1) were monitored for the development of their hypothalamo‐neurohypophysial system as indicated by the kinetics of arginine vasotocin (AVT) gene expression via mRNA concentration and brain AVT content. Our data concerning the onset of gene expression support previous results from our laboratory and others about an early activation of the AVT gene transcriptional and translational activity around E6. We could detect measurable amounts of AVT in chicken embryo brains at E6 and an exponential increase during further development until D1. Dot blots of hypothalamic RNA extracts indicated that AVT gene transcript concentrations rose between E12 and E17 and slightly dropped thereafter. Northern hybridization showed that this drop was caused by a decrease of full length message and an increase of smaller transcripts during late embryonal and D1 stages, probably an AVT mRNA specific degradation phenomenon. The dissociation between the increase of AVT concentration and AVT mRNA concentration visible at the D1 stage might be due to accumulation and storage of AVT in the magnocellular neurons, preferentially in their axon terminals in the neurohypophysis. Blood samples taken from E14 onwards revealed a constant increase in plasma osmolality and plasma AVT concentration. Our data suggest that, in the chicken, AVT seems to be required early during embryonal development, either for osmoregulatory or further unknown functions.
Fos Expression in the Rat Brain Following Vaginal‐Cervical Stimulation by Mating and Manual Probing
Authors: Tetel Marc J. , Getzinger Michael J. , Blaustein Jeffrey D. 
Published: September 2006

AbstractVaginal‐cervical stimulation (VCS), provided by mating or manual probing, induces many reproductive behavioral and endocrine changes in female rats. These changes include an increase in lordosis duration, heat termination and pseudopregnancy. Electro‐physiological and [14C]2‐deoxy‐D‐glucose studies collectively show that neurons in the medial preoptic area, ventromedial hypothalamus and midbrain central gray respond to manual VCS. In the present study we immunocytochemically labeled brain sections for Fos, the protein product of the immediate early gene c‐fos, to detect VCS‐responsive neurons in hormone‐primed animals receiving VCS by mating or manual probing. In Experiment 1, females receiving mounts and intromissions were compared to: 1) vaginally‐masked females receiving mounts but no VCS, 2) females exposed to an intact anesthetized male or 3) females not exposed to males or the testing arena. Those animals receiving VCS showed a dramatic increase in the number of Fos‐immunoreactive cells in the medial preoptic area, posterodorsal portion of the medial amygdala and bed nucleus of the stria terminalis, as well as the dorsomedial hypothalamus, ventromedial hypothalamus and midbrain central gray. These effects of VCS were confirmed in Experiment 2 in animals receiving manual vaginal‐cervical probing. These findings extend previous electrophysiological and [14C]2‐deoxy‐D‐glucose studies by providing evidence that additional brain areas respond to VCS by mating, as well as manual probing.
Chronic but not Acute Exposure to Stress is Associated with Hypothalamic Vasoactive Intestinal Polypeptide (VIP) Release into Median Eminence
Authors: Gavalda Amadeu , Benyassi Ahmed , Arancibia Sandor , Armario Antonio 
Published: September 2006

AbstractThe influence of stress on hypothalamic VIP release into the pituitary portal blood has not been assessed at present despite the fact that this peptide has been implicated in the control of several pituitary hormones and especially in the release of prolactin (PRL) caused by stress. In the present work the effect of stress on the in vivo release of VIP into the pituitary portal blood of male rats was evaluated by means of push‐pull perfusion (PPP) of median eminence (ME). VIP content in the PPP liquid was successfully measured and their levels agree well with pituitary portal blood levels measured by other authors. Whereas plasma PRL levels strongly increased during acute immobilization (IMO), no changes in VIP secretion into the ME were observed. VIP release into the ME was also unaffected by exposure to ether. In contrast, in chronically immobilized rats a significant increase in VIP release into the ME was obtained in response to acute IMO. The present data argue against a major role of hypothalamic VIP in PRL release caused by acute stress and show that chronic stress qualitatively alters the signal of hypothalamic VIP to the pituitary.
Inhibitory Effects of Natriuretic Peptides on Vasopressin Neurons Mediated through cGMP and cGMP‐Dependent Protein Kinase in vitro
Authors: Akamatsu Naoki , Inenaga Kiyotoshi , Yamashita Hiroshi 
Published: September 2006

AbstractThe effects of natriuretic peptides on electrical activity and cellular cGMP levels were studied in neurons of the supraoptic nucleus (SON) of rat hypothalamic slice preparations. Intracellular and extracellular recordings showed that bath application of A type natriuretic peptide (ANP) at 100 nM or B type natriuretic peptide (BNP) at 100 to 300 nM decreased the firing rate and hyperpolarized the membrane potential in phasically firing (putative vasopressin) neurons. Non‐phasically firing (putative oxytocin) neurons did not respond to these natriuretic peptides in firing rate or membrane potential. The membrane‐permeable cGMP analogue 8‐bromo cGMP at 0.5 mM and the phosphodiesterase inhibitor 3‐isobutyl‐1‐methylxanthine (IBMX) at 50 μM mimicked the inhibitory effects of ANP and BNP. The specific inhibitor of cGMP phosphodiesterase 1‐(3‐chloroanilino)‐4‐phenylphthalazine (MY5445) at 30 μM also decreased the firing rate of SON neurons. The cGMP‐dependent protein kinase inhibitor N‐(2‐(methylamino)ethyl)‐5‐isoquinoline‐sulfonamide dihydrochloride (H8) at 1 μM abolished the inhibition by natriuretic peptides. We measured cGMP and cAMP contents in discrete SON regions and compared the change of the contents before and after application of ANP and BNP. The increases in cellular cGMP accumulation were 430% for ANP and 120% for BNP, although they did not cause significant change of cAMP accumulation. The results suggest that the inhibitory effects of natriuretic peptides on putative vasopressin neurons are mediated through cGMP and cGMP‐dependent protein kinase.
Effects of Morphine and Naloxone on Prolactin and Growth Hormone Gene Expression in the Male Rat Pituitary Gland
Authors: Dobado‐Berrios Pablo‐Manuel , Li Songuyn , de Yebenes Ester Garcia , Pelletier Georges 
Published: September 2006

AbstractIt is generally admitted that opioids can stimulate the release of both prolactin (PRL) and growth hormone (GH). In order to investigate the role of opioids in the regulation of PRL and GH gene expression in the rat pituitary, we studied the effects of chronic administration of the opioid drug morphine and an opiate receptor antagonist naloxone on both PRL and GH gene expression as measured by in situ hybridization. Four‐day treatment with morphine (40 mg/kg/day) produced a 12% increase in PRL mRNA levels. Conversely, naloxone (4 mg/kg/day) decreased the autoradiographic reaction by 10%. The concomitant administration of morphine and naloxone induced no significant changes in PRL gene expression. On the other hand, treatment with morphine produced a 22% decrease in GH mRNA levels, an effect which was prevented by the concomitant administration of naloxone. When injected alone, naloxone did not modify the hybridization signal. These results clearly indicate that opioids are involved not only in the regulation of GH and PRL release but also in the gene expression of the two hormones. The discordance observed between the acute effects of morphine on GH release and the effect of the opioid drug on mRNA levels remains to be clarified.