Oxytocin Using ALZET Osmotic Pumps
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Oxytocin Is an Anabolic Bone Hormone
Oxytocin is an anabolic bone hormone Roberto Tammaa,1, Graziana Colaiannia,1, Ling-ling Zhub, Adriana DiBenedettoa, Giovanni Grecoa, Gabriella Montemurroa, Nicola Patanoa, Maurizio Strippolia, Rosaria Vergaria, Lucia Mancinia, Silvia Coluccia, Maria Granoa, Roberta Faccioa, Xuan Liub, Jianhua Lib, Sabah Usmanib, Marilyn Bacharc, Itai Babc, Katsuhiko Nishimorid, Larry J. Younge, Christoph Buettnerb, Jameel Iqbalb, Li Sunb, Mone Zaidib,2, and Alberta Zallonea,2 aDepartment of Human Anatomy and Histology, University of Bari, 70124 Bari, Italy; bThe Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY 10029; cBone Laboratory, The Hebrew University of Jerusalem, Jerusalem 91120, Israel; dGraduate School of Agricultural Science, Tohoku University, Aoba-ku, Sendai, Miyagi 981-8555 Japan; and eCenter for Behavioral Neuroscience, Department of Psychiatry, Emory University School of Medicine, Atlanta, GA 30322 Communicated by Maria Iandolo New, Mount Sinai School of Medicine, New York, NY, February 19, 2009 (received for review October 24, 2008) We report that oxytocin (OT), a primitive neurohypophyseal hor- null mice (5). But the mice are not rendered diabetic, and serum mone, hitherto thought solely to modulate lactation and social glucose homeostasis remains unaltered (9). Thus, whereas the bonding, is a direct regulator of bone mass. Deletion of OT or the effects of OT on lactation and parturition are hormonal, actions OT receptor (Oxtr) in male or female mice causes osteoporosis that mediate appetite and social bonding are exerted centrally. resulting from reduced bone formation. Consistent with low bone The precise neural networks underlying OT’s central effects formation, OT stimulates the differentiation of osteoblasts to a remain unclear; nonetheless, one component of this network mineralizing phenotype by causing the up-regulation of BMP-2, might be the interactions between leptin- and OT-ergic neurones which in turn controls Schnurri-2 and 3, Osterix, and ATF-4 expres- in the hypothalamus (10). -
Secretin and Autism: a Clue but Not a Cure
SCIENCE & MEDICINE Secretin and Autism: A Clue But Not a Cure by Clarence E. Schutt, Ph.D. he world of autism has been shaken by NBC’s broadcast connections could not be found. on Dateline of a film segment documenting the effect of Tsecretin on restoring speech and sociability to autistic chil- The answer was provided nearly one hundred years ago by dren. At first blush, it seems unlikely that an intestinal hormone Bayless and Starling, who discovered that it is not nerve signals, regulating bicarbonate levels in the stomach in response to a but rather a novel substance that stimulates secretion from the good meal might influence the language centers of the brain so cells forming the intestinal mucosa. They called this substance profoundly. However, recent discoveries in neurobiology sug- “secretin.” They suggested that there could be many such cir- gest several ways of thinking about the secretin-autism connec- culating substances, or molecules, and they named them “hor- tion that could lead to the breakthroughs we dream about. mones” based on the Greek verb meaning “to excite”. As a parent with more than a decade of experience in consider- A simple analogy might help. If the body is regarded as a commu- ing a steady stream of claims of successful treatments, and as a nity of mutual service providers—the heart and muscles are the pri- scientist who believes that autism is a neurobiological disorder, I mary engines of movement, the stomach breaks down foods for have learned to temper my hopes about specific treatments by distribution, the liver detoxifies, and so on—then the need for a sys- seeing if I could construct plausible neurobiological mechanisms tem of messages conveyed by the blood becomes clear. -
Oxytocin Effects in Mothers and Infants During Breastfeeding
© 2013 SNL All rights reserved REVIEW Oxytocin effects in mothers and infants during breastfeeding Oxytocin integrates the function of several body systems and exerts many effects in mothers and infants during breastfeeding. This article explains the pathways of oxytocin release and reviews how oxytocin can affect behaviour due to its parallel release into the blood circulation and the brain. Oxytocin levels are higher in the infant than in the mother and these levels are affected by mode of birth. The importance of skin-to-skin contact and its association with breastfeeding and mother-infant bonding is discussed. Kerstin Uvnäs Moberg Oxytocin – a system activator increased function of inhibitory alpha-2 3 MD, PhD xytocin, a small peptide of just nine adrenoceptors . Professor of Physiology amino acids, is normally associated The regulation of the release of oxytocin Swedish University of Agriculture O with labour and the milk ejection reflex. is complex and can be affected by different [email protected] However, oxytocin is not only a hormone types of sensory inputs, by hormones such Danielle K. Prime but also a neurotransmitter and a as oestrogen and even by the oxytocin 1,2 molecule itself. This article will focus on PhD paracrine substance in the brain . During Breastfeeding Research Associate breastfeeding it is released into the brain of four major sensory input nervous Medela AG, Baar, Switzerland both mother and infant where it induces a pathways (FIGURES 2 and 3) activated by: great variety of functional responses. 1. Sucking of the mother’s nipple, in which Through three different release pathways the sensory nerves originate in the (FIGURE 1), oxytocin functions rather like a breast. -
Physiology of Hypothalamus and Pituitary
Physiology of Hypothalamus and Pituitary Simge Aykan, PhD Department of Physiology Ankara University School of Medicine Pituitary Gland • Pituitary gland (hypophysis) is two different tissue types that merged during embryonic development • Anterior pituitary (adenohypophysis): true endocrine gland of epithelial origin • Posterior pituitary (neurohypophysis): extension of the neural tissue of the brain • secretes neurohormones made in the hypothalamus Pituitary Gland • Pituitary bridges and integrates the neural and endocrine mechanisms of homeostasis. • Highly vascular • Posterior pituitary receives arterial blood • anterior pituitary receives only portal venous inflow from the median eminence. • Portal system is particularly important in its function of carrying neuropeptides from the hypothalamus and pituitary stalk to the anterior pituitary. Posterior Pituitary • Storage and release site for two neurohormones (peptide hormones) • Oxytocin • Vasopressin (antidiuretic hormone; ADH) • Large diameter neurons producing hormones are clustered in hypothalamus at paraventricular (oxytocin) and supraoptic nuclei (ADH) • Secretory vesicles containing neurohormones transported to posterior pituitary through axons of the neurons • Stored at the axons until a release signal arrives • Depolarization of the axon terminal opens voltage gated Ca2+ channels and exocytosis is triggered • Hormones release to the circulation Posterior Pituitary • The posterior pituitary regulates water balance and uterine contraction • Vasopressin (ADH), is a neuropeptide -
Transition from Biological to Chemical Assay for Quality Assurance of Medicinal Substances (Apis) and Formulated Preparations
WHO/BS/07.2070 ENGLISH ONLY EXPERT COMMITTEE ON BIOLOGICAL STANDARDIZATION Geneva - 8 to 12 October 2007 Discussion paper: Transition from biological to chemical assay for quality assurance of medicinal substances (APIs) and formulated preparations A Bristow National Institute for Biological Standards and Control, Blanche Lane, South Mimms, Potters Bar, Herts EN6 3QG, UK ML Rabouhans, J Joung, DJ Wood World Health Organization, Geneva, Switzerland © World Health Organization 2007 All rights reserved. Publications of the World Health Organization can be obtained from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; e-mail: [email protected] ). Requests for permission to reproduce or translate WHO publications – whether for sale or for noncommercial distribution – should be addressed to WHO Press, at the above address (fax: +41 22 791 4806; e-mail: [email protected] ). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters. -
Oxytocin to Accelerate Or Induce Labour
CLINICAL PRACTICE GUIDELINE OXYTOCIN CLINICAL PRACTICE GUIDELINE OXYTOCIN TO ACCELERATE OR INDUCE LABOUR Institute of Obstetricians and Gynaecologists, Royal College of Physicians of Ireland and the Clinical Strategy and Programmes Division, Health Service Executive Version: 1.0 Publication date: April 2016 Guideline No: 36 Revision date: April 2019 CLINICAL PRACTICE GUIDELINE OXYTOCIN Table of Contents 1. Revision History ....................................................................................................................... 3 2. Key recommendations .......................................................................................................... 3 3. Purpose and Scope ................................................................................................................. 4 4. Background ............................................................................................................................... 5 5. Methodology .............................................................................................................................. 9 6. Clinical guideline ................................................................................................................... 10 7. References .............................................................................................................................. 16 8. Implementation Strategy ................................................................................................... 19 9. Key Performance Indicators ............................................................................................ -
Understanding Peptide Binding in Class a G Protein-Coupled Receptors
Molecular Pharmacology Fast Forward. Published on July 10, 2019 as DOI: 10.1124/mol.119.115915 This article has not been copyedited and formatted. The final version may differ from this version. MOL# 115915 Understanding peptide binding in Class A G protein-coupled receptors Irina G. Tikhonova, Veronique Gigoux, Daniel Fourmy School of Pharmacy, Medical Biology Centre, Queen’s University Belfast, Belfast BT9 7BL, Northern Ireland, United Kingdom, (I.G.T.) INSERM ERL1226-Receptology and Therapeutic Targeting of Cancers, Laboratoire de Physique et Chimie des Nano-Objets, CNRS UMR5215-INSA, Université de Toulouse III, F- 31432 Toulouse, France. (V.G., D.F.) Downloaded from molpharm.aspetjournals.org Keywords: peptides, peptide GPCRs, peptide binding at ASPET Journals on September 30, 2021 1 Molecular Pharmacology Fast Forward. Published on July 10, 2019 as DOI: 10.1124/mol.119.115915 This article has not been copyedited and formatted. The final version may differ from this version. MOL# 115915 Running title page: Peptide Class A GPCRs Corresponding author: Irina G. Tikhonova School of Pharmacy, Medical Biology Centre, 97 Lisburn Road, Queen’s University Belfast, Belfast BT9 7BL, Northern Ireland, United Kingdom Email: [email protected] Tel: +44 (0)28 9097 2202 Downloaded from Number of text pages: 10 Number of figures: 3 molpharm.aspetjournals.org Number of references: 118 Number of tables: 2 Words in Abstract: 163 Words in Introduction: 503 Words in Concluding Remarks: 661 at ASPET Journals on September 30, 2021 ABBREVIATIONS: AT1, -
Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease
cells Review Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease Chongxu Zhang 1, Tengjiao Cui 1, Renzhi Cai 1, Medhi Wangpaichitr 1, Mehdi Mirsaeidi 1,2 , Andrew V. Schally 1,2,3 and Robert M. Jackson 1,2,* 1 Research Service, Miami VAHS, Miami, FL 33125, USA; [email protected] (C.Z.); [email protected] (T.C.); [email protected] (R.C.); [email protected] (M.W.); [email protected] (M.M.); [email protected] (A.V.S.) 2 Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33101, USA 3 Department of Pathology and Sylvester Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33101, USA * Correspondence: [email protected]; Tel.: +305-575-3548 or +305-632-2687 Received: 25 August 2020; Accepted: 17 October 2020; Published: 21 October 2020 Abstract: Growth hormone-releasing hormone (GHRH) is secreted primarily from the hypothalamus, but other tissues, including the lungs, produce it locally. GHRH stimulates the release and secretion of growth hormone (GH) by the pituitary and regulates the production of GH and hepatic insulin-like growth factor-1 (IGF-1). Pituitary-type GHRH-receptors (GHRH-R) are expressed in human lungs, indicating that GHRH or GH could participate in lung development, growth, and repair. GHRH-R antagonists (i.e., synthetic peptides), which we have tested in various models, exert growth-inhibitory effects in lung cancer cells in vitro and in vivo in addition to having anti-inflammatory, anti-oxidative, and pro-apoptotic effects. One antagonist of the GHRH-R used in recent studies reviewed here, MIA-602, lessens both inflammation and fibrosis in a mouse model of bleomycin lung injury. -
Inhibition of Gastrin Release by Secretin Is Mediated by Somatostatin in Cultured Rat Antral Mucosa
Inhibition of gastrin release by secretin is mediated by somatostatin in cultured rat antral mucosa. M M Wolfe, … , G M Reel, J E McGuigan J Clin Invest. 1983;72(5):1586-1593. https://doi.org/10.1172/JCI111117. Research Article Somatostatin-containing cells have been shown to be in close anatomic proximity to gastrin-producing cells in rat antral mucosa. The present studies were directed to examine the effect of secretin on carbachol-stimulated gastrin release and to assess the potential role of somatostatin in mediating this effect. Rat antral mucosa was cultured at 37 degrees C in Krebs-Henseleit buffer, pH 7.4, gassed with 95% O2-5% CO2. After 1 h the culture medium was decanted and mucosal gastrin and somatostatin were extracted. Carbachol (2.5 X 10(-6) M) in the culture medium increased gastrin level in the medium from 14.1 +/- 2.5 to 26.9 +/- 3.0 ng/mg tissue protein (P less than 0.02), and decreased somatostatin-like immunoreactivity in the medium from 1.91 +/- 0.28 to 0.62 +/- 0.12 ng/mg (P less than 0.01) and extracted mucosal somatostatin-like immunoreactivity from 2.60 +/- 0.30 to 1.52 +/- 0.16 ng/mg (P less than 0.001). Rat antral mucosa was then cultured in the presence of secretin to determine its effect on carbachol-stimulated gastrin release. Inclusion of secretin (10(-9)-10(-7) M) inhibited significantly carbachol-stimulated gastrin release into the medium, decreasing gastrin from 26.9 +/- 3.0 to 13.6 +/- 3.2 ng/mg (10(-9) M secretin) (P less than 0.05), to 11.9 +/- 1.7 ng/mg (10(-8) secretin) (P less than 0.02), and to 10.8 +/- 4.0 ng/mg (10(-7) M secretin) (P less than […] Find the latest version: https://jci.me/111117/pdf Inhibition of Gastrin Release by Secretin Is Mediated by Somatostatin in Cultured Rat Antral Mucosa M. -
In Vivo Electrophysiology of Peptidergic Neurons In
International Journal of Molecular Sciences Article In Vivo Electrophysiology of Peptidergic Neurons in Deep Layers of the Lumbar Spinal Cord after Optogenetic Stimulation of Hypothalamic Paraventricular Oxytocin Neurons in Rats Daisuke Uta 1,*,†, Takumi Oti 2,3,† , Tatsuya Sakamoto 3 and Hirotaka Sakamoto 3,* 1 Department of Applied Pharmacology, Faculty of Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan 2 Department of Biological Sciences, Faculty of Science, Kanagawa University, Hiratsuka, Kanagawa 259-1293, Japan; [email protected] 3 Ushimado Marine Institute (UMI), Graduate School of Natural Science and Technology, Okayama University, Ushimado, Setouchi, Okayama 701-4303, Japan; [email protected] * Correspondence: [email protected] (D.U.); [email protected] (H.S.); Tel.: +81-76-434-7513 (D.U.); +81-869-34-5210 (H.S.) † Authors with equal contributions. Abstract: The spinal ejaculation generator (SEG) is located in the central gray (lamina X) of the rat lumbar spinal cord and plays a pivotal role in the ejaculatory reflex. We recently reported that SEG neurons express the oxytocin receptor and are activated by oxytocin projections from the paraventricular nucleus of hypothalamus (PVH). However, it is unknown whether the SEG responds Citation: Uta, D.; Oti, T.; Sakamoto, T.; to oxytocin in vivo. In this study, we analyzed the characteristics of the brain–spinal cord neural Sakamoto, H. In Vivo Electrophysiology circuit that controls male sexual function using a newly developed in vivo electrophysiological of Peptidergic Neurons in Deep Layers technique. Optogenetic stimulation of the PVH of rats expressing channel rhodopsin under the of the Lumbar Spinal Cord after oxytocin receptor promoter increased the spontaneous firing of most lamina X SEG neurons. -
Secretin/Vasoactive Intestinal Peptide-Stimulated Secretion of Bombesin/ Gastrin Releasing Peptide from Human Small Cell Carcinoma of the Lung1
ICANCER RESEARCH 46, 1214-1218, March 1986] Secretin/Vasoactive Intestinal Peptide-stimulated Secretion of Bombesin/ Gastrin Releasing Peptide from Human Small Cell Carcinoma of the Lung1 Louis Y. Korman,2 Desmond N. Carney, Marc L. Citron, and Terry W. Moody Medica/ Service (151W), Veterans Administration Medical Center, Washington, DC 20422 [L. Y.K., M.L.C.]; Department of Medicine and Biochemistry George Washington University School of Medicine, Washington, DC 20037 [T. W. M.¡;and National Cancer Institute-Navy Medical Oncology Branch National Cancer Institute and National Naval Medical Center, Bethesda, Maryland [D. N. C.¡ ABSTRACT autocrine factor for SCCL (12) growth. We studied the mecha nism of BLI secretion in several SCCL cell lines by examining Bombesin/gastrin releasing peptide-like immunoreactivity (BLI) the action of agents that increase intracellular cAMP. is found in the majority of small cell carcinoma of the lung (SCCL) Because of the results of these in vitro studies and the fact cell lines examined. Because BLI is present in high concentration that secretin stimulates hormone release in patients with gastrin in SCCL we studied the mechanism of BLI secretion from several producing tumors (Zollinger-Ellison syndrome), we examined the SCCL cell lines and in patients with SCCL. In cell line NCI-H345 action of i.v. secretin infusion on plasma BLI levels in several the structurally related polypeptide hormones secretin, vasoac- patients with SCCL, non-SCCL lung tumors, and patients with tive intestinal peptide, and peptide histidine isoleucine as well as theophylline, a phosphodiesterase inhibitor, N6,O2'-dibutyryl out any cancer. cyclic adenosine 3':5'-monophosphate, a cyclic nucleotide ana logue, increased BLI release by 16-120% and cyclic adenosine MATERIALS AND METHODS 3':5'-monophosphate by 36-350%. -
Opioid Modulation of Oxytocin Release
Review Opioid Modulation of Oxytocin Release Mark S. Morris, BA, Edward F. Domino, MD, and Steven E. Domino, MD Analgesia or anesthesia is frequently used for women in of a labor without sufficient cervical dilatation. This labor. A wide range of opioid analgesics with vastly differ- review discusses the scientific basis for opioid modulation ent pharmacokinetics, potencies, and potential side effects of oxytocin release from the posterior pituitary and the can be considered by physicians and midwives for labor- practical implications of this relationship to explain well- ing patients requesting pain relief other than a labor epi- known clinical observations of the effect of morphine on dural. The past 50 years have seen the use of the classic prodromal labor. mu opioid agonist morphine and other opioids diminish markedly for several reasons, including availability of Keywords: endogenous opioids; morphine; meperidine; epidural anesthetics, side effects, formulary restrictions, mu-kappa-delta opioid receptors; oxytocin; and concern for neonatal respiratory depression. Morphine parturition; vasopressin is now primarily used in obstetrics to provide rest and Journal of Clinical Pharmacology, 2010;50:1112-1117 sedation as appropriate for the stressed prodromal stages © 2010 The Author(s) he major hormone involved with parturition to system in modulating oxytocin release, it is of inter- Tstimulate uterine contractions is oxytocin. est to note the use of exogenous mu opioids such as Russell et al1 have reviewed the extensive literature morphine and meperidine in human parturition. on the complexity of the magnocellular oxytocin Different forms of analgesia/anesthesia are needed system. Endogenous opioids mechanisms inhibit for both the benefit of the woman in labor and her oxytocin release as part of the multiple hormones baby.