Oxytocin Effects in Mothers and Infants During Breastfeeding
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The Baseline Structure of the Enteric Nervous System and Its Role in Parkinson’S Disease
life Review The Baseline Structure of the Enteric Nervous System and Its Role in Parkinson’s Disease Gianfranco Natale 1,2,* , Larisa Ryskalin 1 , Gabriele Morucci 1 , Gloria Lazzeri 1, Alessandro Frati 3,4 and Francesco Fornai 1,4 1 Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56126 Pisa, Italy; [email protected] (L.R.); [email protected] (G.M.); [email protected] (G.L.); [email protected] (F.F.) 2 Museum of Human Anatomy “Filippo Civinini”, University of Pisa, 56126 Pisa, Italy 3 Neurosurgery Division, Human Neurosciences Department, Sapienza University of Rome, 00135 Rome, Italy; [email protected] 4 Istituto di Ricovero e Cura a Carattere Scientifico (I.R.C.C.S.) Neuromed, 86077 Pozzilli, Italy * Correspondence: [email protected] Abstract: The gastrointestinal (GI) tract is provided with a peculiar nervous network, known as the enteric nervous system (ENS), which is dedicated to the fine control of digestive functions. This forms a complex network, which includes several types of neurons, as well as glial cells. Despite extensive studies, a comprehensive classification of these neurons is still lacking. The complexity of ENS is magnified by a multiple control of the central nervous system, and bidirectional communication between various central nervous areas and the gut occurs. This lends substance to the complexity of the microbiota–gut–brain axis, which represents the network governing homeostasis through nervous, endocrine, immune, and metabolic pathways. The present manuscript is dedicated to Citation: Natale, G.; Ryskalin, L.; identifying various neuronal cytotypes belonging to ENS in baseline conditions. -
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). -
Neurotransmitter Actions
Central University of South Bihar Panchanpur, Gaya, India E-Learning Resources Department of Biotechnology NB: These materials are taken/borrowed/modified/compiled from various resources like research articles and freely available internet websites, and are meant to be used solely for the teaching purpose in a public university, and for serving the needs of specified educational programmes. Dr. Jawaid Ahsan Assistant Professor Department of Biotechnology Central University of South Bihar (CUSB) Course Code: MSBTN2003E04 Course Name: Neuroscience Neurotransmitter Actions • Excitatory Action: – A neurotransmitter that puts a neuron closer to an action potential (facilitation) or causes an action potential • Inhibitory Action: – A neurotransmitter that moves a neuron further away from an action potential • Response of neuron: – Responds according to the sum of all the neurotransmitters received at one time Neurotransmitters • Acetylcholine • Monoamines – modified amino acids • Amino acids • Neuropeptides- short chains of amino acids • Depression: – Caused by the imbalances of neurotransmitters • Many drugs imitate neurotransmitters – Ex: Prozac, zoloft, alcohol, drugs, tobacco Release of Neurotransmitters • When an action potential reaches the end of an axon, Ca+ channels in the neuron open • Causes Ca+ to rush in – Cause the synaptic vesicles to fuse with the cell membrane – Release the neurotransmitters into the synaptic cleft • After binding, neurotransmitters will either: – Be destroyed in the synaptic cleft OR – Taken back in to surrounding neurons (reuptake) Excitable cells: Definition: Refers to the ability of some cells to be electrically excited resulting in the generation of action potentials. Neurons, muscle cells (skeletal, cardiac, and smooth), and some endocrine cells (e.g., insulin- releasing pancreatic β cells) are excitable cells. -
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 -
Oxytocinergic-System-A-Proposal.Pdf
Opinion Article iMedPub Journals ACTA PSYCHOPATHOLOGICA 2018 www.imedpub.com ISSN 2469-6676 Vol.4 No.3:14 DOI: 10.4172/2469-6676.100170 Oxytocinergic System: A Proposal João Paulo Correia Lima* and Avelino Luiz Rodrigues Received: April 17, 2018; Accepted: May 07, 2018; Published: May 18, 2018 Department of Clinical Psychology and Nucleus of Neuroscience and Behavior, Institute of Psychology, University of Sao Introduction Paulo, Brazil Since 1910, when Ott and Scott [1] published their discovers about the oxytocin participation in milk ejection, the comprehension *Corresponding author: about function and role of oxytocin in several physiological João Paulo Correia Lima functions didn’t stop enlarging and growing. In birth, through his action over uterus contractions, in uterus contractions in [email protected] women’s orgasm and men’s erection [2,3], for instance. However, this approach always considers its peripheral effects. After this, Psychologist for Neuroscience and Behavior, some oxytocin effects had been reported to have actions over Institute of Psychology, University of Sao behavioural traits, like we can see in publishings of Pedersen and Paulo, Brazil. Prange [4] and Winslow and co-workers [5], reporting the oxytocin actions over, respectively, maternal behaviour and pair bonding. Tel: +55-11-32852420; +55-11-983439754 Since then, the increasing data about the oxytocin’s function in behaviour and its central action can’t be ignored. In this short proposal, we’ll consider the opportunity or utility of thinking Citation about oxytocin as a system, instead of a single neurotransmitter. : Lima JPC, Rodrigues AL (2018) Oxytocinergic System: A Proposal. Acta Neurotransmitter or Hormone: Central Psychopathol Vol.4 No.3:14 and Peripheral Actions of Oxytocin Once a molecule could have his function defined through the way death, passive avoidance). -
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, -
Neuroscience: the Science of the Brain
NEUROSCIENCE SCIENCE OF THE BRAIN AN INTRODUCTION FOR YOUNG STUDENTS British Neuroscience Association European Dana Alliance for the Brain Neuroscience: the Science of the Brain 1 The Nervous System P2 2 Neurons and the Action Potential P4 3 Chemical Messengers P7 4 Drugs and the Brain P9 5 Touch and Pain P11 6 Vision P14 Inside our heads, weighing about 1.5 kg, is an astonishing living organ consisting of 7 Movement P19 billions of tiny cells. It enables us to sense the world around us, to think and to talk. The human brain is the most complex organ of the body, and arguably the most 8 The Developing P22 complex thing on earth. This booklet is an introduction for young students. Nervous System In this booklet, we describe what we know about how the brain works and how much 9 Dyslexia P25 there still is to learn. Its study involves scientists and medical doctors from many disciplines, ranging from molecular biology through to experimental psychology, as well as the disciplines of anatomy, physiology and pharmacology. Their shared 10 Plasticity P27 interest has led to a new discipline called neuroscience - the science of the brain. 11 Learning and Memory P30 The brain described in our booklet can do a lot but not everything. It has nerve cells - its building blocks - and these are connected together in networks. These 12 Stress P35 networks are in a constant state of electrical and chemical activity. The brain we describe can see and feel. It can sense pain and its chemical tricks help control the uncomfortable effects of pain. -
Mechanism for Neurotransmitter-Receptor Matching
Mechanism for neurotransmitter-receptor matching Dena R. Hammond-Weinbergera,1,2, Yunxin Wanga, Alex Glavis-Blooma, and Nicholas C. Spitzera,b,1 aNeurobiology Section, Division of Biological Sciences, University of California San Diego, La Jolla, CA 92093-0357; and bCenter for Neural Circuits and Behavior, Kavli Institute for Brain and Mind, University of California San Diego, La Jolla, CA 92161 Contributed by Nicholas C. Spitzer, January 6, 2020 (sent for review September 25, 2019; reviewed by Laura N. Borodinsky and Joshua R. Sanes) Synaptic communication requires the expression of functional neurons lead to the appearance of functional neuromuscular postsynaptic receptors that match the presynaptically released junctions expressing GluR1 and GluR2 (alias GluA1 and GluA2) neurotransmitter. The ability of neurons to switch the transmitter subunits, which are blocked by the AMPA receptor antagonist they release is increasingly well documented, and these switches GYKI 52466 (16, 17). In the central nervous system, the natural require changes in the postsynaptic receptor population. Al- developmental transmitter switch from GABA to glycine in the though the activity-dependent molecular mechanism of neuro- auditory nervous system is accompanied by alterations in the transmitter switching is increasingly well understood, the basis properties of postsynaptic receptors (18, 19). Changes in illumi- of specification of postsynaptic neurotransmitter receptors match- nation during development or in photoperiod in the adult lead to ing the newly expressed transmitter is unknown. Using a func- changes in the numbers of neurons expressing dopamine in the tional assay, we show that sustained application of glutamate to embryonic vertebrate skeletal muscle cells cultured before hypothalamus that are accompanied by corresponding up- or innervation is necessary and sufficient to up-regulate ionotropic down-regulation of dopamine receptor expression in postsynaptic glutamate receptors from a pool of different receptors expressed neurons (5, 7). -
Neurotransmitter Notes
Synapses and Neurotransmitters Notes Chemical Transmitters called “Neurotransmitters” carry a signal across Synapses (& at Neuromuscular Junctions) A point of contact between two neurons is called a synapse At the synapse there is a break in electrical transmission (the action potential cannot cross). Instead chemicals called “neurotransmitters” are released that carry the signal to the next nerve. There is a delay at synapses, because chemical transmission between neurons is slower than electrical transmission (action potential) within a neuron. A neuromuscular junction (NMJ) is a contact between a neuron and a muscle: it is like a synapse in that the action potential stops and the signal is carried by a chemical neurotransmitter released by the neuron. Neurotransmitters Are Made and Stored in the Pre-synaptic Terminal The end of the neuron enlarges into an axon terminal Neurotransmitters are produced in the cell body of a neuron and then transported to the ends of the axon terminals in small membrane-enclosed sacs called “synaptic vesicles”. At the axon terminus, neurotransmitters are stored in these tiny synaptic vesicles so that they can be released when an action potential reaches the axon terminus At a synapse, axon termini of the pre-synaptic neuron contact the dendrites of the post-synaptic neuron. Because the neurotransmitter is only located in the axon termini on one side of a synapse, the impulse can go in only one direction. Calcium is Required for Neurotransmitter Release Neurotransmitter release requires Ca2+ ions Normally, the concentration of Ca2+ in the pre-synaptic neuron l is kept very low (by the action of a Ca pump). -
5-HT2C Agonists Modulate Schizophrenia-Like Behaviors in Mice
Neuropsychopharmacology (2017) 42, 2163–2177 © 2017 American College of Neuropsychopharmacology. All rights reserved 0893-133X/17 www.neuropsychopharmacology.org 5-HT2C Agonists Modulate Schizophrenia-Like Behaviors in Mice 1 1,2 3,7 4 1 Vladimir M Pogorelov , Ramona M Rodriguiz , Jianjun Cheng , Mei Huang , Claire M Schmerberg , 4 5 3 ,1,2,6 Herbert Y Meltzer , Bryan L Roth , Alan P Kozikowski and William C Wetsel* 1 2 Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC, USA; Mouse Behavioral and Neuroendocrine 3 Analysis Core Facility, Duke University Medical Center, Durham, NC, USA; Drug Discovery Program, Department of Medicinal Chemistry and 4 Pharmacognosy, College of Pharmacy, University of Illinois, Chicago, IL, USA; Department of Psychiatry and Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA; 5National Institute of Mental Health Psychoactive Drug Screening Program, Department of Pharmacology and Division of Chemical Biology and Medicinal Chemistry, University of North Carolina Chapel Hill Medical School, Chapel Hill, NC, 6 USA; Departments of Cell Biology and Neurobiology, Duke University Medical Center, Durham, NC, USA All FDA-approved antipsychotic drugs (APDs) target primarily dopamine D2 or serotonin (5-HT2A) receptors, or both; however, these medications are not universally effective, they may produce undesirable side effects, and provide only partial amelioration of negative and cognitive symptoms. The heterogeneity of pharmacological responses in schizophrenic patients suggests that additional drug targets may be effective in improving aspects of this syndrome. Recent evidence suggests that 5-HT receptors may be a promising target for 2C schizophrenia since their activation reduces mesolimbic nigrostriatal dopamine release (which conveys antipsychotic action), they are expressed almost exclusively in CNS, and have weight-loss-promoting capabilities.