Antidepressants Using ALZET Osmotic Pumps
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Antinociceptive Effects of Monoamine Reuptake Inhibitors in Assays of Pain-Stimulated and Pain-Depressed Behaviors
Virginia Commonwealth University VCU Scholars Compass Theses and Dissertations Graduate School 2012 Antinociceptive Effects of Monoamine Reuptake Inhibitors in Assays of Pain-Stimulated and Pain-Depressed Behaviors Marisa Rosenberg Virginia Commonwealth University Follow this and additional works at: https://scholarscompass.vcu.edu/etd Part of the Medical Pharmacology Commons © The Author Downloaded from https://scholarscompass.vcu.edu/etd/2715 This Thesis is brought to you for free and open access by the Graduate School at VCU Scholars Compass. It has been accepted for inclusion in Theses and Dissertations by an authorized administrator of VCU Scholars Compass. For more information, please contact [email protected]. ANTINOCICEPTIVE EFFECTS OF MONOAMINE REUPTAKE INHIBITORS IN ASSAYS OF PAIN-STIMULATED AND PAIN-DEPRESSED BEHAVIOR A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science at Virginia Commonwealth University By Marisa B. Rosenberg Bachelor of Science, Temple University, 2008 Advisor: Sidney Stevens Negus, Ph.D. Professor, Department of Pharmacology/Toxicology Virginia Commonwealth University Richmond, VA May, 2012 Acknowledgement First and foremost, I’d like to thank my advisor Dr. Steven Negus, whose unwavering support, guidance and patience throughout my graduate career has helped me become the scientist I am today. His dedication to education, learning and the scientific process has instilled in me a quest for knowledge that I will continue to pursue in life. His thoroughness, attention to detail and understanding of pharmacology has been exemplary to a young person like me just starting out in the field of science. I’d also like to thank all of my committee members (Drs. -
Emerging Evidence for a Central Epinephrine-Innervated A1- Adrenergic System That Regulates Behavioral Activation and Is Impaired in Depression
Neuropsychopharmacology (2003) 28, 1387–1399 & 2003 Nature Publishing Group All rights reserved 0893-133X/03 $25.00 www.neuropsychopharmacology.org Perspective Emerging Evidence for a Central Epinephrine-Innervated a1- Adrenergic System that Regulates Behavioral Activation and is Impaired in Depression ,1 1 1 1 1 Eric A Stone* , Yan Lin , Helen Rosengarten , H Kenneth Kramer and David Quartermain 1Departments of Psychiatry and Neurology, New York University School of Medicine, New York, NY, USA Currently, most basic and clinical research on depression is focused on either central serotonergic, noradrenergic, or dopaminergic neurotransmission as affected by various etiological and predisposing factors. Recent evidence suggests that there is another system that consists of a subset of brain a1B-adrenoceptors innervated primarily by brain epinephrine (EPI) that potentially modulates the above three monoamine systems in parallel and plays a critical role in depression. The present review covers the evidence for this system and includes findings that brain a -adrenoceptors are instrumental in behavioral activation, are located near the major monoamine cell groups 1 or target areas, receive EPI as their neurotransmitter, are impaired or inhibited in depressed patients or after stress in animal models, and a are restored by a number of antidepressants. This ‘EPI- 1 system’ may therefore represent a new target system for this disorder. Neuropsychopharmacology (2003) 28, 1387–1399, advance online publication, 18 June 2003; doi:10.1038/sj.npp.1300222 Keywords: a1-adrenoceptors; epinephrine; motor activity; depression; inactivity INTRODUCTION monoaminergic systems. This new system appears to be impaired during stress and depression and thus may Depressive illness is currently believed to result from represent a new target for this disorder. -
Strategies for Managing Sexual Dysfunction Induced by Antidepressant Medication
King’s Research Portal DOI: 10.1002/14651858.CD003382.pub3 Document Version Publisher's PDF, also known as Version of record Link to publication record in King's Research Portal Citation for published version (APA): Taylor, M. J., Rudkin, L., Bullemor-Day, P., Lubin, J., Chukwujekwu, C., & Hawton, K. (2013). Strategies for managing sexual dysfunction induced by antidepressant medication. Cochrane Database of Systematic Reviews, (5). https://doi.org/10.1002/14651858.CD003382.pub3 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. -
Diphenhydramine Hydrochloride (CASRN 147-24-0) in F344/N Rats
NATIONAL TOXICOLOGY PROGRAM Technical Report Series No. 355 TOXICOLOGY AND CARCINOGENESIS STUDIES OF DIPHENHYDRAMINE HYDROCHLORIDE (CAS NO. 147-24-0) IN F344/N RATS AND B6C3F1 MICE (FEED STUDIES) LJ.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health NTP ‘TECHNICAL REPORT ON THE TOXICOLOGY AND CARCINOGENESIS STUDIES OF DIPHENHYDRAMINE HYDROCHLORIDE (CAS NO. 147-24-0) IN F344/N RATS AND B6C3F1 MICE (FEED STUDIES) R. Melnick, Ph.D., Study Scientist NATIONAL TOXICOLOGY PROGRAM P.O. Box 12233 Research Triangle Park, NC 27709 September 1989 NTP TR 355 NIH Publication No. 89-2810 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health CONTENTS PAGE ABSTRACT ................................................................ 3 EXPLANATION OF LEVELS OF EVIDENCE OF CARCINOGENIC ACTIVITY .................. 6 CONTRIBUTORS ............................................................ 7 PEERREVIEWPANEL ........................................................ 8 SUMMARY OF PEER REVIEW COMMENTS ......................................... 9 I. INTRODUCTION ........................................................ 11 I1. MATERIALS AND METHODS .............................................. 21 III. RESULTS ............................................................. 35 RATS ............................................................. 36 MICE ............................................................. 45 GENETIC TOXICOLOGY ............................................... 53 IV. -
Novel Approaches for the Treatment of Alzheimer's and Parkinson's Disease
International Journal of Molecular Sciences Review Novel Approaches for the Treatment of Alzheimer’s and Parkinson’s Disease Michiel Van Bulck 1,2 , Ana Sierra-Magro 1,2, Jesus Alarcon-Gil 1, Ana Perez-Castillo 1,2 and Jose A. Morales-Garcia 1,2,3,* 1 Instituto de Investigaciones Biomédicas (CSIC-UAM), Arturo Duperier, 4. 28029 Madrid, Spain; [email protected] (M.V.B.); [email protected] (A.S.-M.); [email protected] (J.A.-G.); [email protected] (A.P.-C.) 2 Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Valderrebollo, 5, 28031 Madrid, Spain 3 Departamento de Biología Celular, Facultad de Medicina, Universidad Complutense de Madrid (UCM), Plaza Ramón y Cajal s/n, 28040 Madrid, Spain * Correspondence: [email protected] Received: 31 December 2018; Accepted: 3 February 2019; Published: 8 February 2019 Abstract: Neurodegenerative disorders affect around one billion people worldwide. They can arise from a combination of genomic, epigenomic, metabolic, and environmental factors. Aging is the leading risk factor for most chronic illnesses of old age, including Alzheimer’s and Parkinson’s diseases. A progressive neurodegenerative process and neuroinflammation occur, and no current therapies can prevent, slow, or halt disease progression. To date, no novel disease-modifying therapies have been shown to provide significant benefit for patients who suffer from these devastating disorders. Therefore, early diagnosis and the discovery of new targets and novel therapies are of upmost importance. Neurodegenerative diseases, like in other age-related disorders, the progression of pathology begins many years before the onset of symptoms. Many efforts in this field have led to the conclusion that exits some similar events among these diseases that can explain why the aging brain is so vulnerable to suffer neurodegenerative diseases. -
Role of Dietary Histidine in the Prevention of Obesity and Metabolic Syndrome
Open access Editorial Open Heart: first published as 10.1136/openhrt-2017-000676 on 1 July 2018. Downloaded from Role of dietary histidine in the prevention of obesity and metabolic syndrome James J DiNicolantonio,1 Mark F McCarty,2 James H OKeefe 1 To cite: DiNicolantonio JJ, HISTIDINE SUPPLEMENTATION AMELIORATES histidine dose dependently increases hypo- McCarty MF, OKeefe JH. Role of METABOLIC SYNDROME thalamic levels of histamine as well as hypo- dietary histidine in the prevention of obesity and A recent Chinese supplementation study, in thalamic activity of histidine decarboxylase, metabolic syndrome. Open Heart which obese middle-aged women diagnosed the enzyme which converts histidine to hista- 10 2018;5:e000676. doi:10.1136/ with metabolic syndrome received 12 weeks mine. Such administration also inhibits food openhrt-2017-000676 of supplemental histidine (2 g, twice daily) or consumption—an effect that is blocked in matching placebo, achieved remarkable find- animals pretreated with an irreversible inhib- 1 Accepted 24 April 2018 ings. Insulin sensitivity improved significantly itor of histidine decarboxylase. in the histidine-supplemented subjects, and Neuronal histamine release in the hypo- this may have been partially attributable to thalamus is subject to feedback regulation loss of body fat. Body mass index (BMI), waist by presynaptic H3 receptors. In rodent circumference and body fat declined in the studies, antagonists and inverse agonists for histidine-supplemented group relative to the these receptors have been shown to mark- placebo group; the average fat loss in the histi- edly amplify hypothalamic histamine levels, dine group was a robust 2.71 kg. Markers of suppress feeding, decrease body weight and systemic inflammation such as serum tumour enhance metabolic rate.11–15 Such agents may necrosis factor-alpha (TNF-α) and inter- have clinical potential for managing obesity. -
(19) United States (12) Patent Application Publication (10) Pub
US 20130289061A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2013/0289061 A1 Bhide et al. (43) Pub. Date: Oct. 31, 2013 (54) METHODS AND COMPOSITIONS TO Publication Classi?cation PREVENT ADDICTION (51) Int. Cl. (71) Applicant: The General Hospital Corporation, A61K 31/485 (2006-01) Boston’ MA (Us) A61K 31/4458 (2006.01) (52) U.S. Cl. (72) Inventors: Pradeep G. Bhide; Peabody, MA (US); CPC """"" " A61K31/485 (201301); ‘4161223011? Jmm‘“ Zhu’ Ansm’ MA. (Us); USPC ......... .. 514/282; 514/317; 514/654; 514/618; Thomas J. Spencer; Carhsle; MA (US); 514/279 Joseph Biederman; Brookline; MA (Us) (57) ABSTRACT Disclosed herein is a method of reducing or preventing the development of aversion to a CNS stimulant in a subject (21) App1_ NO_; 13/924,815 comprising; administering a therapeutic amount of the neu rological stimulant and administering an antagonist of the kappa opioid receptor; to thereby reduce or prevent the devel - . opment of aversion to the CNS stimulant in the subject. Also (22) Flled' Jun‘ 24’ 2013 disclosed is a method of reducing or preventing the develop ment of addiction to a CNS stimulant in a subj ect; comprising; _ _ administering the CNS stimulant and administering a mu Related U‘s‘ Apphcatlon Data opioid receptor antagonist to thereby reduce or prevent the (63) Continuation of application NO 13/389,959, ?led on development of addiction to the CNS stimulant in the subject. Apt 27’ 2012’ ?led as application NO_ PCT/US2010/ Also disclosed are pharmaceutical compositions comprising 045486 on Aug' 13 2010' a central nervous system stimulant and an opioid receptor ’ antagonist. -
52Nd Annual Meeting
ACNP 52nd Annual Meeting Final Program December 8-12, 2013 The Westin Diplomat Resort & Spa Hollywood, Florida President: David A. Lewis, M.D. Program Committee Chair: Randy D. Blakely, Ph.D. Program Committee Co-Chair: Pat R. Levitt, Ph.D. This meeting is jointly sponsored by the Vanderbilt University School of Medicine Department of Psychiatry and the American College of Neuropsychopharmacology. Dear ACNP Members and Guests, It is a distinct pleasure to welcome you to the 2014 meeting of the American College of Neuropsychopharmacology! This 52nd annual meeting will again provide opportunities for the exercise of the College’s core values: the spirit of Collegiality, promoting in each other the best in science, training and service; participation in Community, pursuing together the goals of understanding the neurobiology of brain diseases and eliminating their burden on individuals and our society; and engaging in Celebration, taking the time to recognize and enjoy the contributions and accomplishments of our members and guests. Under the excellent leadership of Randy Blakely and Pat Levitt, the Program Committee has done a superb job in assembling an outstanding slate of scientific presentations. Based on membership feedback, the meeting schedule has been designed with the goals of achieving an optimal mix of topics and types of sessions, increasing the diversity of participating scientists and creating more time for informal interactions. The presentations will highlight both the breadth of the investigative interests of ACNP membership -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
Pharmacological Characterizations of H05, a Novel Potent Serotonin And
JPET/2018/248351 Title: Pharmacological characterization of (3-(benzo[d][1,3] dioxol-4-yloxy) -3-(4-fluorophenyl)-N, N-dimethylpropan-1-amine (H05), a novel serotonin and noradrenaline reuptake inhibitor with moderate 5-HT2A antagonist activity for the treatment of depression Authors: Xiangqing Xu, Yaqin Wei, Qiang Guo, Song Zhao, Zhiqiang Liu, Ting Xiao, Yani Liu, Yinli Qiu, Yuanyuan Hou, Guisen Zhang and KeWei Wang Affiliations: Department of Molecular and Cellular Pharmacology, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University , Beijing, China (X.X., T.X., K.W.W.); School of pharmacy, Xuzhou Medical University, Xuzhou, Jiangsu, China (Y.W.); Institute of pharmaceutical research, Jiangsu Nhwa Pharmaceutical Co., Ltd., Xuzhou, Jiangsu, China (Q.G., S.Z., Z.L., Y.Q., Y.H., G.Z.); Department of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, Shandong, China (Y.L., K.W.W.) 1 Running title page Running title: A novel SNRI with 5-HT2A antagonist activity for treatment of depression Corresponding author: KeWei Wang Address: No. 38 Xueyuan Road, Haidian District, Beijing, 100191, China. Tel: 86•10•82805605; E•mail: [email protected] or [email protected] Number of text pages: 57 Number of tables: 3 Number of figures: 7 Number of references: 71 Words in Abstract: 248 Words in Introduction: 712 Words in Discussion:1357 Abbreviations: ADs: antidepressants; SSRIs: selective serotonin reuptake inhibitors; NRIs: norepinephrine reuptake inhibitors; SNRIs: serotonin and norepinephrine -
Intrinsic Cardiac Catecholamines Help Maintain Beating Activity in Neonatal Rat Cardiomyocyte Cultures
0031-3998/04/5603-0411 PEDIATRIC RESEARCH Vol. 56, No. 3, 2004 Copyright © 2004 International Pediatric Research Foundation, Inc. Printed in U.S.A. Intrinsic Cardiac Catecholamines Help Maintain Beating Activity in Neonatal Rat Cardiomyocyte Cultures ARUNA R. NATARAJAN, QI RONG, ALEXANDER N. KATCHMAN, AND STEVEN N. EBERT Department of Pediatrics [A.R.N.], Department of Pharmacology [Q.R., A.N.K., S.N.E.], Georgetown University Medical Center, Washington, DC 20057, U.S.A. ABSTRACT In the present study, we identify intrinsic cardiac adrenergic indicate that intrinsic cardiac catecholamines help to maintain (ICA) cells in the neonatal rat heart using immunofluorescent beating rates in neonatal rat cardiomyocyte cultures via stimula- ␣  histochemical staining techniques with antibodies that specifi- tion of 1- and -adrenergic receptors. This information should cally recognize the major enzymes in the catecholamine biosyn- help to increase our understanding of the physiologic mecha- thetic pathway. ICA cells are most concentrated near the endo- nisms governing cardiovascular function in neonates. (Pediatr cardial surface of ventricular myocardium, but are also found Res 56: 411–417, 2004) sporadically throughout the heart. In primary cultures of neonatal rat cardiomyocytes, ICA cells are closely associated with clusters Abbreviations of cardiomyocytes. To investigate a potential role for intrinsi- ICA, intrinsic cardiac adrenergic cally produced catecholamines, we recorded beating rates in the TH, tyrosine hydroxylase presence and absence of the catecholamine-depleting agent re- DBH, dopamine -hydroxylase serpine or the adrenergic receptor blockers prazosin and timolol PNMT, phenylethanolamine N-methyltransferase using videomicroscopy and photodiode sensors. Our results TRITC, tetramethylrhodamine isothiocyanate show that beating rates slow significantly when endogenous DOPS, dihydroxyphenylserine catecholamines are depleted or when their action is blocked with DMEM, Dulbecco’s modified Eagle medium  ␣ either a -oran 1-adrenergic receptor antagonist. -
PHARMACEUTICAL APPENDIX to the TARIFF SCHEDULE 2 Table 1
Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE HARMONIZED TARIFF SCHEDULE Harmonized Tariff Schedule of the United States (2020) Revision 19 Annotated for Statistical Reporting Purposes PHARMACEUTICAL APPENDIX TO THE TARIFF SCHEDULE 2 Table 1. This table enumerates products described by International Non-proprietary Names INN which shall be entered free of duty under general note 13 to the tariff schedule. The Chemical Abstracts Service CAS registry numbers also set forth in this table are included to assist in the identification of the products concerned. For purposes of the tariff schedule, any references to a product enumerated in this table includes such product by whatever name known.