bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypophysiotropic Role and Hypothalamic Gene Expression of Corticotropin‐Releasing Factor and Vasopressin in Rats Injected with Interleukin‐1β Systemically or into the Brain Ventricles
Authors: Lee Soon , Rivier Catherine 
Published: September 2006

AbstractIntact adult male rats were injected intravenously (i.v., 400 ng/kg), intraperitoneally (i.p., 400 ng/kg) or intracerebroventricularly (i.c.v., 100 ng/kg) with interleukin‐1β (IL‐1β) or its vehicle. In comparison with vehicle‐treated animals, IL‐1β induced significant (P<0.01) increases in plasma ACTH levels measured 30 min later regardless of the route of cytokine administration. These changes were markedly blunted in rats administered specific antibodies directed against corticotropin‐releasing factor (CRF). In contrast, vasopressin (VP) antibodies significantly blunted ACTH released by the i.c.v. injection of IL‐1β, but only modestly altered the effect of the systemic injection of the cytokine. We then used semi‐quantitative in situ hybridization analysis to measure changes in steady‐state mRNA levels, as they might occur in response to these same doses of IL‐1β. Following administration of the vehicle, measurement of gene expression in the paraventricular (PVN) portion of the hypothalamus indicated a measurable amount of hybridization signals for both CRF and VP. No detectable changes in either CRF or VP gene expression were observed in rats injected with IL‐1β i.v. or i.p. 5 h earlier. In contrast, the i.c.v. administration of the cytokine significantly (P<0.01) increased both CRF and VP mRNA levels measured 5 h later.These results suggest that while endogenous CRF modulates the response of the corticotrophs to this cytokine regardless of the route of administration, the role of VP is more important in rats injected centrally than in those injected peripherally. The observation that at the dose tested and over the time‐course studied, systemic injection of IL‐1β failed to alter CRF or VP gene expression, supports our earlier hypothesis that blood‐born IL‐1β acts primarily at the level of nerve terminals in the median eminence.
The Neuroendocrinology of the Adrenal Cortex
Authors: Vinson G. P. , Hinson J. P. , Tóth I. E. 
Published: September 2006

AbstractAlthough until relatively recently assumed to be devoid of innervation, there is now ample proof that the adrenal cortex receives specific neurones of several types. A general interpretation of their roles in the regulation of adrenocortical function has not been forthcoming, probably because of the variety of the different experimental approaches which have been used, and the heterogeneous observations which have been made. We here summarize the evidence which is available, and offer the view that neural inputs may provide fine tuning of the responses to systemic factors such as ACTH, through direct actions on specific adrenocortical cells. However, neural regulation also provides an integrative function, through actions on the flow of blood through the gland, which itself exerts a powerful influence on adrenocortical function.
Glucocorticoids Regulate Hippocampal 11β‐Hydroxysteroid Dehydrogenase Activity and Gene Expression in vivo in the Rat
Authors: Low Susan C. , Moisan Marie‐Pierre , Noble June M. , Edwards Christopher R. W. , Seckl Jonathan R. 
Published: September 2006

AbstractChronic glucocorticoid excess or deficiency is associated with hippocampal dysfunction and neuronal death. 11β‐hydroxysteroid dehydro‐genase (11β‐OHSD), which catalyses the reversible conversion of corticosterone to inactive 11 ‐dehydrocorticosterone, regulates glucocorticoid access to receptors in the kidney and liver in vivo. The enzyme is also present in the hippocampus where it might modulate glucocorticoid action. We examined the effects of corticosteroid manipulations on hippocampal and peripheral 11β‐OHSD. In the hippocampus, chronic adrenalectomy (10 days) had no effect on 11β‐OHSD activity, compared to sham‐operated controls. Treatment of adrenalectomized animals with dexamethasone (200 μg/kg.day−1), but not aldosterone (20 μg/kg.day−1), for 10 days significantly increased hippocampal 11β‐OHSD activity compared with sham or adrenalectomized rats (22% and 23% rise respectively, P<0.05). These effects reflect changes in transcription of the liver‐type 11β‐OHSD gene, with dexamethasone significantly increasing 11β‐OHSD mRNA expression in the hippocampus compared with sham or adrenalectomized animals (32% and 70% higher respectively, P<0.05). In the liver, adrenalectomy significantly reduced 11β‐OHSD activity (16% lower), which was restored to sham levels by dexamethasone, but not aldosterone. Similar trends were seen in 11β‐OHSD mRNA expression, although these did not reach significance. None of the manipulations altered 11β‐OHSD activity or mRNA expression in the kidney. The hippocampal effects of dexamethasone were similar to those of chronic stress (arthritis) which increased 11β‐OHSD activity (20% rise, P<0.05), although this was not reflected at the level of mRNA. Thus, hippocampal (and hepatic, but not renal) 11β‐OHSD appears to be regulated by chronic glucocorticoid manipulations and stress. Hippocampal 11β‐OHSD may thus ensure optimal long‐term corticosterone exposure of glucocorticoid‐sensitive neurons.
Regulation of Pituitary Vasopressin Receptors during Chronic Stress: Relationship to Corticotroph Responsiveness
Authors: Aguilera Greti , Pham Quocan , Rabadan‐Diehl Cristina 
Published: September 2006

AbstractThe relationship between vasopressin (VP) receptor levels in the anterior pituitary and VP‐stimulated ACTH release in vitro was studied in rats subjected to various chronic stress paradigms. The stress models used were water deprivation for 60 h and administration of 2% NaCI in the drinking water (both of which are associated with decreased pituitary ACTH responsiveness), and repeated i.p.hypertonic saline injections or repeated daily immobilization for 14 days (associated with increased ACTH responsiveness to novel stimuli). VP receptors were measured by binding of [3H]arginine‐VP to anterior pituitary membrane‐rich fractions, and ACTH responses to VP in collagenase dispersed anterior pituitary cells. In control rats, binding of [3H]AVP was saturable and high affinity, with a Kd of 0.45 ± 0.05 nM and a Bmax of 138.8 ± 8.1 fmol/mg. In pituitary membranes from stressed rats, binding affinity was unchanged, but Bmax changed according to the type of stress. While VP binding was markedly reduced after water deprivation and 2% saline (25% and 49%, respectively), it was significantly increased after repeated i.p. hypertonic saline injections and repeated immobilization (126% and 154% of controls, respectively). The changes in VP binding were associated to parallel changes in maximum VP‐stimulated ACTH production in vitro, with a 34% decrease in water deprived rats and a 25% increase in hypertonic saline injected rats. The potentiating effect of VP on corticotropin releasing hormone‐stimulated ACTH was also reduced in cells from water‐restricted rats, and increased in cells from rats given repeated injections of hypertonic saline. The data show a direct relationship between changes in corticotroph responsiveness and changes in pituitary VP receptors during chronic stress, suggesting that pituitary VP receptor regulation is involved in the adaptation of the HPA axis during chronic stress.
Prenatal Stress Increases the Hypothalamo‐Pituitary‐Adrenal Axis Response in Young and Adult Rats
Authors: Henry Chantal , Kabbaj Mohamed , Simon Hervé , Le Moal Michel , Maccari Stefania 
Published: September 2006

AbstractPrenatal stress is considered as an early epigenetic factor able to induce long‐lasting alterations in brain structures and functions. It is still unclear whether prenatal stress can induce long‐lasting modifications in the hypothalamo‐pituitary‐adrenal axis. To test this possibility the effects of restraint stress in pregnant rats during the third week of gestation were investigated in the functional properties of the hypothalamo‐pituitary‐adrenal axis and hippocampal type I and type II corticosteroid receptors in the male offspring at 3, 21 and 90 days of age. Plasma corticosterone was significantly elevated in prenatally‐stressed rats at 3 and 21 days after exposure to novelty. At 90 days of age, prenatally‐stressed rats showed a longer duration of corticosterone secretion after exposure to novelty. No change was observed for type I and type II receptor densities 3 days after birth, but both receptor subtypes were decreased in the hippocampus of prenatally‐stressed offspring at 21 and 90 days of life. These findings suggest that prenatal stress produces long term changes in the hypothalamo‐pituitary‐adrenal axis in the offspring.
Simultaneous Monitoring of Intracerebral Release and Behavior: Endogenous Vasopressin Improves Social Recognition
Authors: Engelmann Mario , Ludwig Mike , Landgraf Rainer 
Published: September 2006

AbstractWe previously reported that direct osmotic stimulation of the supraoptic nucleus (SON) of rats via a microdialysis probe produces a robust ‘rebound’ release of endogenous vasopressin (AVP) into the extracellular fluid of this hypothalamic nucleus (1). We now demonstrate in a combined microdialysis and push‐pull perfusion study that this intranuclear release is accompanied by increased AVP release in the septum. Simultaneous monitoring of intranuclear release and behavioral performance in the same animal indicated a significant correlation between the amount of endogenously released AVP and improved social memory based on the olfactory discriminative capacities of adult male rats. This memory improvement was partially blocked by local administration of a AVP V1 receptor antagonist either into the SON or septum. These findings indicate that direct osmotic stimulation of the supraoptic nucleus, which increases intracerebral vasopressin release, improves the acquisition and/or processing of olfactory stimuli. Thus, the endogenous neuropeptide fulfills one of the major criteria for being causally involved as a neurotransmitter/neuromodulator in behavioral performance.
Androgen Receptor Function During Undernutrition
Authors: Dong Qihan , Rintala Harri , Handelsman David J 
Published: September 2006

AbstractHypothalamo‐pituitary inhibition of reproductive function during undernutrition is well known, however, the physiological mechanisms leading to suppression of gonadotrophin secretion are not clear. A variety of studies have indicated that testicular negative feedback on LH secretion is enhanced during food restriction. To evaluate directly the suppression by endogenous androgens on hypothalamic GnRH pulse generator activity during food restriction and examine the mechanism underlying the increased testicular steroidal feedback, we examined (1) circulating bioactive LH (bLH) levels in response to selective cerebral androgen blockade by intraventricular administration of an androgen receptor antagonist (hydroxyflutamide, SCH 16423) and (2) the binding capacity and affinity of androgen receptors in medio‐basal hypothalamus, pituitary and prostate during undernutrition of intact mature male rats. Hydroxyflutamide (20 μg in 10μl vehicle), but not vehicle alone, markedly increased bLH levels in both food restricted and ad‐lib fed rats. However, the faster (geometric mean 11.4 vs 27.7 min) and greater (47.2 vs 21.9 ng/ml) increase in bLH level in food restricted compared with ad‐lib fed controls demonstrates an enhanced sensitivity to blockade of androgenic negative feedback during undernutrition. Food restriction increased androgen receptor binding capacity in pituitary (3.36 vs 0.77fmol/mg protein) but not in medio‐basal hypothalamus or prostate while binding affinity was unchanged by undernutrition in all 3 tissues. These studies reveal that undernutrition both enhances tonic, androgen receptor‐mediated feedback suppression of GnRH secretion and increases in pituitary (but not hypothalamic) androgen receptor numbers to cause inhibition of LH secretion.
Glutamate Inhibits Ingestive Behaviour
Authors: Bednar I. , Qian M. , Qureshi G. A. , Källström L , Johnson A. E. , Carrer H. , Södersten P. 
Published: September 2006

AbstractMale rats treated with reserpine were motionless and ingested only a few of ten consecutive intraoral injections of a 1 M solution of sucrose. While injection of apomorphine, a dopamine agonist, stimulated locomotion and stereotyped sniffing in reserpinized rats, it did not reactivate ingestive responses. The non‐competitive N‐methyl‐D‐aspartate receptor antagonist MK801, however, stimulated locomotion as well as ingestion suggesting involvement of glutamate in the suppressive effect of resperpine on ingestive responses. A series of experiments was therefore undertaken to investigate the possible physiological role of glutamate in feeding.For this purpose, we used Grill's intraoral intake test, in which the rat is infused intraorally with a sucrose solution and the amount ingested measured. In untreated rats, MK801 dose‐dependently facilitated ingestion of the sucrose solution and antagonized inhibition of ingestion by cholecystokinin octapeptide. Administration of cholecystokinin octapeptide or ingestion of sucrose increased the concentration of glutamate in the nucleus of the solitary tract, a brain stem relay transmitting sensory information from the gastrointestinal tract to the forebrain. MK801 was found to bind specifically to this brain area and block the elevation of glutamate and dopamine levels which occurred after treatment with cholecystokinin octapeptide in this neural site. Together these data suggest that dopamine and glutamate may interact within the nucleus of the solitary tract in controlling ingestive behaviour.
Testosterone Implants in Specific Neural Sites Activate Female Sexual Behaviour
Authors: Sharma Usha R. , Rissman Emilie F. 
Published: September 2006

AbstractSexual behaviour in most female mammals is regulated by oestrogen, often acting synergistically with progesterone. Moreover, the most important neural site of action for oestradiol is the ventromedial nucleus. In the female musk shrew, Suncus murinus, testosterone (T) activates sexual behaviour. Virgin females first engage in copulatory behaviour many hours in advance of follicular development and ovulation, when plasma oestradiol levels are very low. Testosterone, produced by the ovaries and the adrenal glands, must be aromatized centrally to oestradiol to initiate sexual behaviour. To identify the neural sites of action for T, ovariectomized females received unilateral hormone implants containing testosterone propionate. Hormone pellets were placed in 1 of several brain sites including the medial preoptic area and the dorsalmedial hypothalamus (DMH). Implants in either of these 2 sites, but not in the lateral preoptic area, internal capsule, nor anterior hypothalamus stimulated the induction of sexual behaviour. Hormone implants in the ventrolateral hypothalamus resulted in partially receptive animals. Immunocytochemistry was employed to determine which steroid receptors were present in the 2 behaviourally active sites. The medial preoptic area (MPO) and the dorsal and ventromedial hypothalamus both contain many cells that express oestrogen receptor immunoreactivity. A smaller subset of neurons in these regions are immunoreactive for androgen receptors. In summary, testosterone can act specifically in either the MPO or the DMH to induce female sexual behaviour. Both sites contain cells that express oestrogen and androgen receptors. Thus, testosterone may work via one or both of these steroid receptors to regulate behaviour. The results of these studies, and data collected previously, show that female sexual behaviour in this species is regulated by T and that this steroid can induce full sexual behaviour in 2 specific neural sites. Both of the sites of action identified in this experiment are critical for the expression of sexual behaviour in other species. The MPO has been shown to regulate male sexual behaviour via the aromatization of T to oestradiol in rodents and birds. The DMH is just dorsal to the ventromedial nucleus (VMN) which is essential for the regulation of sexual behaviour in female rodents. Further work is needed to determine if the neural circuitry for sexual behaviour in the musk shrew involves either the MPO or the VMN, if both areas are essential, or perhaps, the 2 regions regulate different aspects of female sexual behaviour.
Involvement of the Bed Nucleus of the Stria Terminalis in Tonic Regulation of Paraventricular Hypothalamic CRH and AVP mRNA Expression
Authors: Herman James P. , Cullinan William E. , Watson Stanley J. 
Published: September 2006

AbstractThe bed nucleus of the stria terminalis (BNST) occupies a central position in pathways regulating hypothalamo‐pituitary‐adrenocortical (HPA) stress regulation. The potential role of the BNST in tonic neural control of HPA function was assessed by examining effects of selective BNST lesions on expression of ACTH secretagogues in HPA‐integrative neurons of the medial parvocellular paraventricular nucleus. Anterior BNST lesions (ABN) involved major portions of the anteromedial, anterolateral, ventromedial, ventrolateral, dorsolateral and juxtacapsular subnuclei. These lesions resulted in significant (30%) decreases in corticotropin‐releasing hormone (CRH) mRNA expression across the rostrocaudal extent of the medial parvocellular PVN, with no accompanying changes in basal arginine vasopressin (AVP) mRNA levels. Posterior BNST (PBN) lesions involved large but subtotal damage to the posterior intermediate, posterior medial, posterior lateral and preoptic subnuclei; these lesions resulted in small but significant changes in CRH mRNA and slight increases in number of AVP mRNA‐producing parvocellular neurons. PBN effects on CRH mRNA expression were most pronounced at the caudal extent of the medial parvocellular zone, suggesting a topographic input from the posterior BNST to the PVN that is only partially compromised by PBN lesions. Analysis of individual cases revealed a correlation between damage of the anterolateral BNST and decreased CRH mRNA levels, and damage of the posterior intermediate and/or posterior medial BNST and increased CRH mRNA levels. The results suggest differential BNST input into HPA regulation, perhaps reflecting the diversity of limbic input into the BNST region.
Bicuculline Methiodide Influences the Central Nervous System to Produce Hyperglycemia in Rats
Authors: Nonogaki Katsunori , Iguchi Akihisa , Sakamoto Nobuo 
Published: September 2006

AbstractThe influence of bicuculline methiodide (BMI), a gamma‐aminobutyric acid (GABA) receptor antagonist, on central nervous system regulation of blood glucose homeostasis was studied in fed rats. Injection of BMI (1–10 nmol) into the third ventricle was found to produce hepatic venous hyperglycemia in a dose‐dependent manner. This change was associated with increased secretion of epinephrine and glucagon. The role of epinephrine in hyperglycemia was then studied in bilaterally adrenalectomized (ADX) rats injected with BMI. Plasma glucose concentration was found to increase in ADX rats although the level was approximately half that for intact rats and significantly higher than for controls. The increase in epinephrine and glucagon secretion seen in intact rats, but not in ADX rats, suggests BMI‐induced epinephrine release is responsible for the glucagon secretion. Three possible mechanisms are suggested to account for the rise in plasma glucose in the hepatic vein after injection of BMI: 1) that epinephrine is secreted by the adrenal medulla, 2) that epinephrine secretion stimulates glucagon secretion or 3) that there may be some direct innervation of the liver in rats.
Evidence for Multiple Forms of Melatonin Receptor‐G‐Protein Complexes by Solubilization and Gel Electrophoresis
Authors: Barrett P. , MacLean A. , Morgan P. J. 
Published: September 2006

AbstractThe daily production of melatonin from the pineal gland influences circadian and seasonal behaviour and physiology. To further understand how melatonin may function, it is important to characterize the receptor and signal transduction systems. Using the detergent digitonin, we were able to solubilize the receptor from the ovine pars tuberalis (PT) membrane. The receptor was isolated as a complex associated with its heterotrimeric G‐protein. In the solubilized state, pre‐bound 125l‐2‐iodomelatonin was stable at 4°C, but was displaceable by GTPγS. The receptor‐G‐protein complex could be separated by molecular mass using native polyacrylamide gel electrophoresis. We demonstrate that the receptor‐complex has a molecular mass of 525 kDa and differs from solubilized receptor‐complexes isolated from either the lizard brain, chicken brain or the ovine hippocampus. Furthermore the receptor complex isolated from the hippocampus had the lowest molecular mass of these tissues (365 kDa) and was found not to be sensitive to GTPγS. This may indicate the existence of a distinct non‐G‐protein coupled form of the receptor.
The Effects of Aging and Hormonal Manipulation on Amyloid Precursor Protein APP695 mRNA Expression in the Rat Hippocampus
Authors: Chao Helen M. , Spencer Robert L. , Frankfurt Maya , McEwen Bruce S. 
Published: September 2006

AbstractIn the rat hippocampus, neuronal morphology and survival are profoundly affected by adrenal steroids, and synaptic plasticity can be modulated by the ovarian sex steroids estrogen and progesterone, β‐amyloid peptides, which accumulate in neuritic plaques and are derived from the amyloid precursor protein (APR), have been shown to be both trophic and toxic for hippocampal neurons. Of the various APR isoforms, APP695 is the predominant form found in rat brain and the APP695 mRNA is abundantly expressed in the hippocampus. In order to investigate the hypothesis that APR may serve as a mediator of the steroid effects, we have monitored the hippocampal expression of APP695 mRNA by in situ hybridization, with aging and with steroid manipulation. In aged female rats we observed a decrease in the level of APP695 mRNA relative to young female rats, while no such age difference was evident in male rats. Physiological, surgical and pharmacological manipulation of glucocorticoids appeared to have no effect on APP695 mRNA levels in the hippocampus. Treatment of young, ovariectomized female rats with estrogen and progesterone, resulted in an increase in hippocampal APP695 expression compared to untreated, ovariectomized controls.