UNIPROT:P01178 - FACTA Search

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Query: UNIPROT:P01178 (oxytocin)
15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently, novel peptides have been identified as unknown ligands of orphan G-protein coupled receptors. In the paraventicular (PVN) and supraoptic nuclei (SON), the expression of the G-protein genes are abundant. In this review, we focus on the physiological role of neuromedin U and galanin-like peptide, which were recently identified as ligands of G-protein coupled receptors, in the regulation of neurohypophysial hormones. Intracerebroventricular (i.c.v) administration of neuromedin U induced the expression of c-fos mRNA in both the magnocellular and parvocellular division of the PVN and throughout the SON. Administration of i.c.v. neuromedin U caused a significant increase in plasma concentrations of vasopressin and oxytocin as well as adrenocorticotropic hormone. The expression of galanin-like peptide mRNA was observed in the pituicytes of rat posterior pituitary gland. The expression of galanin-like peptide mRNA in the posterior pituitary gland was markedly increased after dehydration, salt loading and intraperitoneal administration of lipopolysaccaride, challenges that stimulate the secretion of vasopressin and oxytocin, and which activate the hypothalamic-pituitary adrenal axis. These results suggest that neuromedin U and galanin-like peptide may have an important role in the regulation of both the hypothalamic-neurohypophysial system and the hypothalamic-adrenohypophysial system.
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PMID:Novel G-protein coupled receptor ligands and neurohypophysial hormones. 1508 78

The present study examined the effect of estradiol on hypothalamic serotonin-1A (5-HT(1A)) receptor signaling in female rats. We first examined the time-course effects of a single injection of the 5-HT(1A) receptor agonist (+/-)8-OH-DPAT (5, 15 or 30 min prior to decapitation), and dose response of (+)8-OH-DPAT (50, 100, 200 or 500 microg/kg, s.c.) on plasma hormones in ovariectomized rats that received a daily injection of beta-estradiol 3-benzoate (10 microg/day, s.c.) or vehicle (sesame oil) for 2 days. In vehicle- and estrogen-treated rats, the peak response of hormones occurred at 15 min after injection and the time-course of oxytocin and adrenocorticotropic hormone (ACTH) responses to an injection of 8-OH-DPAT were comparable. However, only the oxytocin response was reduced by estrogen treatment. A second experiment compared the ACTH and oxytocin responses with doses of 50 or 200 microg/kg, s.c. of (+)8-OH-DPAT vs. (+/-)8-OH-DPAT in ovariectomized rats that were treated with oil or beta-estradiol 3-benzoate (10 microg/day, s.c.) for 2 days. (+)8-OH-DPAT and (+/-)8-OH-DPAT produced a similar magnitude of increase in plasma levels of ACTH and oxytocin. Treatment with beta-estradiol 3-benzoate produced a significant and comparable reduction in the oxytocin response to the highest dose (200 microg/kg, s.c.) of both (+)8-OH-DPAT and (+/-)8-OH-DPAT but did not alter the ACTH response to either (+)8-OH-DPAT or (+/-)8-OH-DPAT. In the dose-response experiment, a dose of 50 microg/kg of (+)8-OH-DPAT produced a maximal increase in plasma levels of ACTH, while the maximal oxytocin response was achieved with a dose of 200 microg/kg, s.c. Treatment with beta-estradiol 3-benzoate reduced the maximal oxytocin response to (+)8-OH-DPAT (by 29%) but did not alter the ACTH response to any doses of (+)8-OH-DPAT. To examine potential mechanisms mediating the effects of estrogen on 5-HT(1A) receptor signaling, we measured the levels of Galpha(i), Galpha(o) and Galpha(z) proteins, which couple 5-HT(1A) receptors to their effector enzymes, in two subregions of the hypothalamus. The levels of Galpha(z) protein were reduced in the mediobasal hypothalamus (containing the ventromedial and arcuate nuclei), which mainly expresses estrogen receptor-alpha, but not in the paraventricular hypothalamus, which mainly expresses estrogen receptor-beta. Estradiol reduced the levels of Galpha(i2) and Galpha(i3 )proteins in both hypothalamic regions but did not affect Galpha(i1) levels in either area. Combined, the data suggest that racemic and stereoselective 8-OH-DPAT have similar neuroendocrine effects and that both estrogen receptor-alpha and estrogen receptor-beta mediate the reduction in levels of Galpha(i2,3) proteins.
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PMID:Estrogen reduces serotonin-1A receptor-mediated oxytocin release and Galpha(i/o/z) proteins in the hypothalamus of ovariectomized rats. 1538 10

Neuropeptide B (NPB) was identified to be an endogenous, peptide ligand for the orphan receptors GPR7 and GPR8. Because GPR7 is expressed in rat brain and, in particular, in the hypothalamus, we hypothesized that NPB might interact with neuroendocrine systems that control hormone release from the anterior pituitary gland. No significant effects of NPB were observed on the in vitro releases of prolactin, adrenocorticotropic hormone (ACTH) or growth hormone (GH) when log molar concentrations ranging from 1 pM to 100 nM NPB were incubated with dispersed anterior pituitary cells harvested from male rats. In addition NPB (100 nM) did not alter the concentration response stimulation of prolactin secretion by thyrotropin-releasing hormone, ACTH secretion by corticotropin-releasing factor (CRF) and GH secretion by GH-releasing hormone. However, NPB, when injected into the lateral cerebroventricle (i.c.v.) of conscious, unrestrained male rats, elevated prolactin and corticosterone, and lowered GH levels in circulation. The threshold dose for the effect on corticosterone and prolactin levels was 1.0 nmol, while that for the effect on GH release was 3.0 nmol NPB. Pretreatment with a polyclonal anti-CRF antiserum completely blocked the ability of NPB to stimulate ACTH release and significantly inhibited the effect of NPB on plasma corticosterone levels. NPB administration i.c.v. did not significantly alter plasma vasopressin and oxytocin levels in conscious rats. It did stimulate feeding (minimum effective dose 1.0 nmol) in sated animals in a manner similar to that of the other endogenous ligand for GPR7, neuropeptide W. We conclude that NPB can act in the brain to modulate neuroendocrine signals accessing the anterior pituitary gland, but does not itself act as a releasing or inhibiting factor in the gland, at least with regard to prolactin, ACTH and GH secretion.
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PMID:Central neuropeptide B administration activates stress hormone secretion and stimulates feeding in male rats. 1550 May 44

Galanin-like peptide is a recently identified neuropeptide. We examined the effects of stressful stimuli on expression of c-Fos protein in galanin-like peptide neurons, and the effects of central infusion of galanin-like peptide on release of stress hormones, vasopressin, oxytocin and adrenocorticotropic hormone, in male rats. Foot shock stress induced expression of c-Fos protein in galanin-like peptide neurons in the hypothalamus. Intracerebroventricular injection of galanin-like peptide significantly increased plasma concentrations of vasopressin, oxytocin and adrenocorticotropic hormone. Galanin-like peptide also increased blood pressure, heart rates and plasma glucose concentrations, but significantly changed neither plasma osmolality nor blood haemoglobin concentration. A neuropeptide Y-Y1 receptor antagonist, BIBP3226, did not significantly change galanin-like peptide-induced hormone release. It is possible that galanin-like peptide is involved in vasopressin, oxytocin and adrenocorticotropic hormone release from the pituitary during stress.
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PMID:Galanin-like peptide stimulates vasopressin, oxytocin and adrenocorticotropic hormone release in rats. 1570 28

Social relationships protect against the development of stress-related psychiatric disorders, yet little is known about the neurobiology that regulates this phenomenon. Recent evidence suggests that oxytocin (OT), a neuropeptide involved in social bond formation, may play a role. This experiment investigated the effects of chronic intranasal OT administration on acute stress-induced hypothalamic-pituitary-adrenal (HPA) axis activation in adult female squirrel monkeys. Subjects were randomized to one of two experimental conditions. Monkeys were intranasally administered either 50 microg oxytocin (N = 6 monkeys) or 0 microg oxytocin (N = 6 monkeys)/300 microl saline once a day for eight consecutive days. Immediately after drug administration on the eighth day, all monkeys were exposed to acute social isolation. Blood samples for determinations of adrenocorticotropic hormone (ACTH) and cortisol concentrations were collected after 30 and 90 min of stress exposure. Consistent with an anti-stress effect, OT-treated monkeys exhibited lower ACTH concentrations compared to saline-treated monkeys after 90 min of social isolation (F(1,7) = 6.891; P = 0.034). No drug-related differences in cortisol levels were observed, indicating that OT does not directly attenuate the adrenal stress response. Intranasal peptide administration has been shown to penetrate the central nervous system, and research must determine whether intranasally delivered OT exerts its effect(s) at a pituitary and/or brain level. This primate model offers critical opportunities to improve our understanding of the anti-stress effects of OT and may lead to novel pharmacological treatments for stress-related psychiatric disorders.
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PMID:Intranasal oxytocin administration attenuates the ACTH stress response in monkeys. 1594 3

Previously, we identified that a majority of patients with anorexia nervosa (AN) and bulimia nervosa (BN) as well as some control subjects display autoantibodies (autoAbs) reacting with alpha-melanocyte-stimulating hormone (alpha-MSH) or adrenocorticotropic hormone, melanocortin peptides involved in appetite control and the stress response. In this work, we studied the relevance of such autoAbs to AN and BN. In addition to previously identified neuropeptide autoAbs, the current study revealed the presence of autoAbs reacting with oxytocin (OT) or vasopressin (VP) in both patients and controls. Analysis of serum levels of identified autoAbs showed an increase of IgM autoAbs against alpha-MSH, OT, and VP as well as of IgG autoAbs against VP in AN patients when compared with BN patients and controls. Further, we investigated whether levels of these autoAbs correlated with psychological traits characteristic for eating disorders. We found significantly altered correlations between alpha-MSH autoAb levels and the total Eating Disorder Inventory-2 score, as well as most of its subscale dimensions in AN and BN patients vs. controls. Remarkably, these correlations were opposite in AN vs. BN patients. In contrast, levels of autoAbs reacting with adrenocorticotropic hormone, OT, or VP had only few altered correlations with the Eating Disorder Inventory-2 subscale dimensions in AN and BN patients. Thus, our data reveal that core psychobehavioral abnormalities characteristic for eating disorders correlate with the levels of autoAbs against alpha-MSH, suggesting that AN and BN may be associated with autoAb-mediated dysfunctions of primarily the melanocortin system.
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PMID:Autoantibodies against neuropeptides are associated with psychological traits in eating disorders. 1619 79

Sex and the endocrine system exert a significant influence on the physiology and pathophysiology of the lacrimal gland. The purpose of this article is to briefly review the nature and magnitude of these interactions between sex, hormones and lacrimal tissue, and to address how they may relate to the pathogenesis of aqueous-deficient dry eye. Towards this end, this article has a 3-fold approach: first, to summarize the influence of androgens, estrogens, glucocorticoids, mineralocorticoids, retinoic acid, prolactin, alpha-melanocyte stimulating hormone, adrenocorticotropic hormone, luteinizing hormone, follicle-stimulating hormone, growth hormone, thyroid-stimulating hormone, arginine vasopressin, oxytocin, thyroxine, parathyroid hormone, insulin, glucagon, melatonin, human chorionic gonadotropin and cholecystokinin on the structure and function of the lacrimal gland; second, to discuss the mechanism of action of each hormone on lacrimal tissue; and third, to discuss the clinical relevance of the endocrine-lacrimal gland interrelationship, with a particular focus on each hormone's role (i.e. if relevant) in the development of aqueous-tear deficiency.
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PMID:Tearful relationships? Sex, hormones, the lacrimal gland, and aqueous-deficient dry eye. 1721 82

The effect of six hormones (histamine, serotonin, insulin, epidermal growth factor (EGF), oxytocin and gonadotropin) was studied on the hormone (histamine, serotonin, adrenocorticotropic hormone [ACTH], endorphin and triiodothyronine [T(3)]) content of Tetrahymena. The hormones were given in 10(-9) or 10(-12) M concentrations or as 0.1 and 0.001 I.U. ml(-1) (in the case of oxytocin and gonadotropin) for 1 h. The hormones in picomolar concentration, i.e. at levels which can be present also in natural conditions, influence the amount of other hormones inside the cell. Their effect is not a general one: it is individual, the level of one of the hormones was elevated, while that of the others diminished under the effect of the same hormonal stimulus. Insulin was the only hormone, which influenced the concentration of other hormones in one direction, elevating them. This effect could have a role in the life-saving property of this hormone in Tetrahymena, but the hormones were not studied from this point of view. Usually there is no difference between the effect of the two concentrations used, but there are situations when the effect of the two concentrations is opposite. This means that there is a possible concentration dependence and this could influence differently the cells which are far from or near to the secretor cell. Considering earlier observations, the duration of the treatment can also influence the result. The results give new data to the hormonal regulation at unicellular level (which can be the base of regulation at higher evolutionary levels) and point to the possibility of a hormonal network.
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PMID:Is there a hormonal network in Tetrahymena? A systematic investigation of hormonal effects on the hormone content. 1795 13

The aim of the thesis was to investigate in male Wistar rats, the involvement of serotonin (5-HT) and 5-HT receptors in the regulation of the gene expression of hypothalamic hormones and in the secretion of the pituitary gland hormones prolactin (PRL), adrenocorticotropic hormone (ACTH), vasopressin (AVP) and oxytocin in basal and stress conditions. Furthermore, to study the significance of some distinctive central nuclei in these processes, and the metabolism of 5-HT in the hypothalamus and the dorsal raphe nucleus (DRN). The experiments were focused on (1) determination of involved neurons and nuclei (2) the hypothalamic level and (3) the pituitary gland level of regulation. The studies were typically performed in vivo but some studies were performed in vitro. Stereotactically neurotoxic lesion with 5,7-dihydroxy-5-HT in the dorsal raphe nucleus (DRN) or the hypothalamic paraventricular nucleus (PVN) reduced the ACTH and AVP response to stress, indicating an importance of these structures for this response. In situ hybridization on rat brain slices with oligopeptides showed an increase of corticotropin releasing hormone (CRH) mRNA in the PVN and proopiomelanocortin in the anterior pituitary lobe upon stimulation of the 5-HT1A, 5-HT1B, 5-HT2A and 5-HT2C receptors. Stimulation of 5-HT2A+2C receptors increased AVP mRNA in the PVN but not in the supraoptic nucleus (SON), whereas the level of oxytocin (OT) mRNA was increased both in the SON and the PVN and this effect was in addition mediated via 5-HT1A+1B receptors. Serotonin infused directly into the PVN by microdialysis stimulated local release of AVP. CRH was found to have a major role but not a complete responsibility in the 5-HT-induced release of ACTH, since immunoneutralisation of CRH inhibited the POMC gene expression and the ACTH response and since 5-HT and 5-HT antagonists were able to modulate the ACTH release from anterior pituitary gland cells in vitro. Through the years of investigation, the classification of the 7 main groups of 5-HT receptors (5-HT1 - 5-HT7) has changed due to molecular biological characterisation of the receptors and new receptors have been identified. With a battery of 5-HT agonists and antagonists several pharmacological experiments were performed with systemically or central administration of compounds and radioimmuno assay of plasma for pituitary gland hormone levels. Specific substances were not available for all 5-HT receptors and subreceptors thus some conclusions are a based on combination of experiments. The 5-HT induced PRL response is mediated via 5-HT1A, 5-HT2A, 5-HT2C and 5-HT3 receptors. In addition an involvement of 5-HT1B, 5-HT5 or 5-HT7 receptors seem possible. The ACTH response to 5-HT is mediated via 5-HT1A, 5-HT1B, 5-HT2A and 5-HT2C receptors and an involvement of the 5-HT4, 5-HT5 and 5-HT7 receptors is proposed. Peripheral secretion of AVP upon stimulation with 5-HT is mediated via 5-HT2C, 5-HT4 and 5-HT7 receptors but not 5-HT1A receptors. The secretion of OT is primarily mediated via 5-HT1A, 5-HT2C and 5-HT4 receptors and probably also 5-HT1B, 5-HT2A, 5-HT5A and 5-HT7 receptors. Physical and psychological stress activates hippocampal and hypothalamic 5-HT neurons. In contrast to other stress factors, restraint stress increases the content of 5-HT in the DRN but do not increase the metabolism of 5-HT and does not induce changes in hypothalamic levels of 5-HT. Large variations are found in the literature with different kinds of stress, different measurements and different time schedules. Restraint or ether stress induced secretion of PRL involves 5-HT2 and 5-HT3 receptors, whereas the ACTH secretion is mediated via 5-HT1A, 5-HT2A and 5-HT2C receptors. In the present study restraint stress increased AVP secretion, but opposite findings has reported possibly due to differences in the stress procedure. The 5-HT2, 5-HT3 and 5-HT4 receptor is involved in the AVP response to restraint whereas the OT response involves the 5-HT1A and the 5-HT2 receptor. The 5-HT2 receptor is involved in the OT response to dehydration or haemorrhage, whereas the AVP responses to these stressors probably do not involve 5-HT. It can be concluded that 5-HT is involved in basal and stress-induced regulation of PRL, ACTH, AVP and oxytocin mainly via the 5-HT2A+2C receptors but other receptors are also important but differs from hormone to hormone. Serotonin affect the secretion of CRH and ACTH both at the hypothalamic, pituitary portal and pituitary gland level, and possibly also at the adrenal level.
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PMID:Studies on the neuroendocrine role of serotonin. 1820 78

A number of synthetic peptides are significant commercial or pharmaceutical products, ranging from the dipeptide sugar-substitute aspartame to clinically used hormones, such as oxytocin, adrenocorticotropic hormone, and calcitonin. This unit provides an overview of the field of synthetic peptides and proteins, including their purification. It discusses selecting the solid support and common coupling reagents. Additional information is provided regarding common side reactions and synthesizing modified residues.
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PMID:Introduction to peptide synthesis. 1842 26

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