DOCSLIB.ORG

7 X 11.5 Three Lines.P65

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
7 X 11.5 Three Lines.P65 Cambridge University Press 978-0-521-71413-6 - Antipsychotics and Mood Stabilizers: Stahl’s Essential Psychopharmacology, Third Edition Stephen M. Stahl Index More information Index Page numbers followed by ‘f ’ indicate figures; page numbers followed by ‘t ’ indicate tables. 3PPP, 134f agitation, benzodiazepines for, 188 AAADC (aromatic amino acid decarboxylase), and receptor conformation, 132f 97, 98f agranulocytosis, clozapine and, 164 ABT089, 203 akathisia acetylcholine (ACh), from aripiprazole, 175 in arousal pathways, 150, 152f nigrostriatal pathway dopamine deficiencies and blocked dopamine receptors, 93f and, 31 overactivity, 95 alanine-serine-cysteine transporter (ASC-T), reciprocal relationship with dopamine, 92f glial, 34 acetylcholine-linked mechanisms, 202 alogia, 5, 6t ACP 103, 200 alpha 1 adrenergic receptors ACP-104, 129, 134f atypical antipsychotic agents and, 139f ACR16, 134f and sedation, 151f adipose tissue, insulin resistance in, 141, alpha-1 receptor, antagonism, 94f 144f alpha-2 adrenergic receptors, atypical adolescence antipsychotic agents and, 139f aggressiveness in, 179 alpha 2 antagonists, 168 removal of synaptic connections, 68 alpha-4 beta-2 nicotinic acetylcholine receptor, risperidone for treating psychotic disorders, 203 166 alpha-7-nicotinic cholinergic agonists, affective blunting, 5 202 affective flattening, as SSRI side effect, 110 alpha amino-3-hydroxy-5-methyl-4- affective symptoms isoxazolepropionic acid (AMPA) dorsal vs. ventral regulation, 76f receptors, 40, 40f, 66f mesolimbic dopamine pathway role in, 28 synapses with, 67f multiple disorders impacting, 15f Alzheimer’s disease, 180 pharmacy, 182, 184f cognitive symptoms, 13 in schizophrenia, shared with other disorders, excitotoxicity and, 56, 57f 14 symptoms shared with schizophrenia, 12, 13, aggressive symptom pharmacy, 181f 13f aggressiveness, 10 amantadine, 194 multiple disorders impacting, 15f, 16f amenorrhea, 32, 90 in schizophrenic patients, 13 d-amino acid oxidase (DAO), 38f, 39 219 © Cambridge University Press www.cambridge.org Cambridge University Press 978-0-521-71413-6 - Antipsychotics and Mood Stabilizers: Stahl’s Essential Psychopharmacology, Third Edition Stephen M. Stahl Index More information amisulpride, 130, 134f, 135f, 176, 183 and prolactin, 118f and cardiometabolic risk, 140t risk and benefits of long-term, 95 clinical actions of, 125 in use, 85t and diabetes, 171 as D2 dopamine receptor blockers, 27 for negative symptoms in schizophrenia, 182f first-generation, 83f, 96 pharmacological icon, 177f high doses, 191f and QTc prolongation, 171 links between binding properties and clinical amoxapine (Asendin), 173, 174f actions, 136 AMPA (alpha-amino-3-hydroxy-5-methyl-4- low-potency, and dissociation, 124 isoxazole-priopionic acid) glutamate “off-label” uses, 82 receptors, 64 patient toleration of, 163 and synaptogenesis, 62 pharmacokinetics, 156–162 AMPA-kines, 199 pharmacological properties, 162–179 amphetamines, 44 prescribing information, 82 and dopamine release, 26 prophylactic, 192 response to emotional input, 78 receptor interactions for, 134 and schizophrenia symptoms, 75, 77f sedation as short-term tool, 152f amylin, 204 side effects and compliance, 153f anhedonia, 5, 6t, 30 switching, 185, 187f antagonists, process to avoid, 187f vs. inverse agonist, 105 from sedating to nonsedating, 189f vs. partial agonists, 132f antisocial personality disorder, 13 presynaptic, 199f anxiety disorders anticholinergic agents 5HT1A receptors and, 103f D2 antagonism and, 93f quetiapine for, 168f side effects, 95 anxious mood, 14 antihistamines, 82 anxious self-punishment, 3 atypical, 96 apathy, 3 administration frequency, 122 histamine-1 with 5HT2C antagonism, 141f cardiometabolic risk and, 140t aripiprazole, 129, 130, 134f–136f, 158, 175, 183 cardiometabolic risk management, 145 and cardiometabolic risk, 140t hit-and-run receptor binding properties, as CYP 2D6 substrate, 158, 159f 124f and diabetes, 171 hypothetical action over time, 125f dosage with carbamazepine, 161f, 162 to improve schizophrenia symptoms, 109 pharmacological icon, 176f pharmacological properties, 139f raising levels of, 160f and prolactin, 118f and sedation, 184, 186f properties, 119, 135f switching from sedating agent to, 189 and weight gain risk, 140t and weight gain risk, 140t avoiding sedation and enhancing long-term aromatic amino acid decarboxylase (AAADC), outcome, 155f 97, 98f benzodiazepines to lead in or top off, 188f asenapine, 122f, 200 best practices for monitoring and managing, Asendin (amoxapine), 173, 174f 149f asociality, 5, 6t cardiometabolic risk and, 137–150 assaultiveness, 10 combining two, 191 atorvastatin conventional, 91f impaired, in schizophrenia, 11 vs. atypical, 112f, 114f attention deficit hyperactivity disorder D2 binding of, 123f (ADHD), 180 D2-receptor antagonist, 83 symptoms shared with schizophrenia, 14 hypothetical action over time, 123f attitudes, hostile, 3 muscarinic cholinergic blocking properties, atypical antipsychotic agents, 96 91, 95 administration frequency, 122 pharmacological properties, 82–96 cardiometabolic risk and, 140t 220 Index © Cambridge University Press www.cambridge.org Cambridge University Press 978-0-521-71413-6 - Antipsychotics and Mood Stabilizers: Stahl’s Essential Psychopharmacology, Third Edition Stephen M. Stahl Index More information cardiometabolic risk management, 145 brain. See also circuits clozapine as, 163 dopamine pathways in, 26f, 22–29 vs. conventional, 112f, 114f excitotoxicity in early development, 62f hit-and-run receptor binding properties, 124f insult and schizophrenia, 57 hypothetical action over time, 125f survival of wrong neurons, 59 properties, 119, 139f focus on malfunctioning areas, 16 and weight gain risk, 140t glutamate pathways in, 43f, 41–45 auditory hallucinations, 5 nucleus accumbens as pleasure center, 83 autism, 180 brain circuits, and schizophrenia symptoms, 14 cognitive symptoms, 13 brain damage, 180 irritability in children with, 181 brain-derived neurotrophic factor (BDNF), 58 risperidone for irritability, 166 5HT6 receptors and, 201 avolution, 5, 6t genes coding for, 63f “awakening”, 164, 191 and long-term memory formation, 99 and synapse formation, 62, 65f benzamide antipsychotics, clinical actions of, Brief Psychiatric Rating Scale, 7t 125 burnout benzodiazepines, 153, 155f, 180 of neuronal systems, 28 for aggression management, 181f in schizophrenic patients, 54, 55f for agitation, 188 buspirone, 201 injectable, 179 to lead in or top off antipsychotics, 188f calcium when switching antipsychotics, excessive 189f and excitotoxicity, 58f bifeprunox (DU 127090), 129, 130, 134f–136f, overexcitation and dangerous opening of, 55 177 calcyon, genes for, 73f and cardiometabolic risk, 140t cannabinoid antagonists, 203 and diabetes, 171 carbamazepine (Equetro), 160 in metabolic pharmacy, 183 CYP450 3A4 and discontinuation, 162f metabolized by CYP 3A4, 158 CYP450 3A4 induced by, 161f for obesity, 202 antipsychotic agents and, 143f, 171 pharmacological icon, 178f atypical antipsychotic agents and, 139, 140t and sedation, 186f clozapine and, 164 sedation risk with, 184 low risk antipscychotic agents, 140t bipolar disorder. See also mood stabilizers olanzapine and, 165 bifeprunox for treating, 178 receptors mediating, 139f depressed phase of, 169 cardiovascular disease olanzapine and, 165 atypical antipsychotic agents and, 137 risperidone effectiveness for, 167 risk of, 142f symptoms shared with schizophrenia, 12, 13, cardiovascular side effects, of antipsychotic 13f drugs, 95 ziprasidone for, 170 catabolic enzymes, blame, 3 and dopamine breakdown, 21, 21f blonanserin, 122f and dorsolateral prefrontal cortex, 19f blood pressure genes for, 73f monitoring, 146, 150f CATIE (Clinical Antipsychotic Trials of blunted affect, 6t Intervention Effectiveness), 153f blurred vision, from conventional cerebral cortex, antipsychotics, 92f antipsychotic agent binding to postsynaptic BMY-14802, 200 5HT2A receptors, 114f body mass index (BMI), 142f aggressiveness in, 179 baseline measurement, 149f psychotic illness, symptoms shared with monitoring, 150f schizophrenia, 12, 13, 13f borderline personality disorder, 13, 180 risperidone for, 166 Index 221 © Cambridge University Press www.cambridge.org Cambridge University Press 978-0-521-71413-6 - Antipsychotics and Mood Stabilizers: Stahl’s Essential Psychopharmacology, Third Edition Stephen M. Stahl Index More information chlorpromazine (Thorazine), 82, 85t in schizophrenia, shared with other disorders, cholecystokinin (CCK), 204 13, 14f chorea, dopamine hyperactivity in nigrostriatal serotonin receptors and, 99 pathway and, 31 cognitive symptom pharmacy, 182, 183f CHRNA (alpha-7 nicotinic cholinergic “combos” (combination of medications) receptor), 72f for schizophrenia, 190, 204 circadian rhythms for symptom reduction in psychosis, 179 5HT7 receptors and, 103f communication Cl1007, 134f dysfunction of, 5 Clinical Antipsychotic Trials of Intervention inhibitors, 202 Effectiveness (CATIE), 153f conceptual disorganization, 3 clinical practice conduct disorder, 179 vs. clinical trials, 178 connectivity, genes affecting, 58 symptom treatment, vs. disease treatment, constipation 179 from conventional antipsychotics, 92f Clopixol (zuclopenthixol), 85t and emotion and cognitive symptoms, clozapine, 136f, 157, 157f, 158, 184 17f 5HT6-antagonist properties of, 201 and schizophrenia symptoms, 15 for affective symptoms in schizophrenia, cortical arousal, neurotransmitters of, 152f 183 cortical brainstem glutamate projection, 43f, for aggression
Load more

Recommended publications
  • 5-HT2A/2C Receptor Modulation of Absence Seizures and Characterization of the GHB-Model
    5-HT2A/2C receptor modulation of absence seizures and characterization of the GHB-model A thesis submitted to Cardiff University for the degree of Doctor of Philosophy by Marcello Venzi (MSc) School of Biosciences, Cardiff University, October 2014 Chapter 1 Declaration and Statements This work has not been submitted in substance for any other degree or award at this or any other university or place of learning, nor is being submitted concurrently in candidature for any degree or other award. Signed ………………………………………… (candidate) Date ………………………… STATEMENT 1 This thesis is being submitted in partial fulfillment of the requirements for the degree of PhD . Signed ………………………………………… (candidate) Date ………………………… STATEMENT 2 This thesis is the result of my own independent work/investigation, except where otherwise stated. Other sources are acknowledged by explicit references. The views expressed are my own. Signed ………………………………………… (candidate) Date ………………………… STATEMENT 3 I hereby give consent for my thesis, if accepted, to be available for photocopying and for inter- library loan, and for the title and summary to be made available to outside organisations. Signed ………………………………………… (candidate) Date ………………………… STATEMENT 4: PREVIOUSLY APPROVED BAR ON ACCESS I hereby give consent for my thesis, if accepted, to be available for photocopying and for inter- library loans after expiry of a bar on access previously approved by the Academic Standards & Quality Committee. Signed ………………………………………… (candidate) Date ………………………… II Chapter 1 Summary Absence seizures (ASs) are non-convulsive epileptic events which are common in pediatric and juvenile epilepsies. They consist of EEG generalized spike-and-wave-discharges (SWDs) accompanied by an impairment of consciousness and are expressed within the thalamocortical network.
    [Show full text]
  • WO 2012/148799 Al 1 November 2012 (01.11.2012) P O P C T
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization International Bureau (10) International Publication Number (43) International Publication Date WO 2012/148799 Al 1 November 2012 (01.11.2012) P O P C T (51) International Patent Classification: (81) Designated States (unless otherwise indicated, for every A61K 9/107 (2006.01) A61K 9/00 (2006.01) kind of national protection available): AE, AG, AL, AM, A 61 47/10 (2006.0V) AO, AT, AU, AZ, BA, BB, BG, BH, BR, BW, BY, BZ, CA, CH, CL, CN, CO, CR, CU, CZ, DE, DK, DM, DO, (21) International Application Number: DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, PCT/US2012/034361 HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, (22) International Filing Date: KZ, LA, LC, LK, LR, LS, LT, LU, LY, MA, MD, ME, 20 April 2012 (20.04.2012) MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, OM, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SC, SD, (25) Filing Language: English SE, SG, SK, SL, SM, ST, SV, SY, TH, TJ, TM, TN, TR, (26) Publication Language: English TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (30) Priority Data: (84) Designated States (unless otherwise indicated, for every 61/480,259 28 April 201 1 (28.04.201 1) US kind of regional protection available): ARIPO (BW, GH, GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, SZ, TZ, (71) Applicant (for all designated States except US): BOARD UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, MD, RU, OF REGENTS, THE UNIVERSITY OF TEXAS SYS¬ TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, TEM [US/US]; 201 West 7th St., Austin, TX 78701 (US).
    [Show full text]
  • 货号 英文名称 规格 D50673 A66 2.5Mg,5Mg,100Ul(10Mm/DMSO
    货号 英文名称 规格 D50673 A66 2.5mg,5mg,100ul(10mM/DMSO) D50690 Acadesine 25mg,50mg,1ml(10mM/DMSO) D50691 Acadesine phosphate 10mg,25mg,1ml(10mM/DMSO) D50580 Acemetacin 500mg D50669 Acetohexamide 25mg,50mg,1ml(10mM/DMSO) D50574 Acrivastine 10mg D50409 Actinomycin D 1mg D50409s Actinomycin D (10mM in DMSO) 100ul D50553 Adavosertib 5mg D50619 Adenosine 5'-monophosphate monohydrate 100mg,250mg,1ml(10mM/DMSO) D50412 Adriamycin 10mg,50mg D50412s Adriamycin (10mM in DMSO) 200ul D50381 AEBSF 10mg,100mg D50381s AEBSF solution (10mM) 100ul D50600 Afloqualone 10mg,50mg,1ml(10mM/DMSO) D50575 Alcaftadine 5mg D50556 Alosetron 2.5mg D50557 Alosetron Hydrochloride 100mg D50675 Alpelisib 5mg,10mg,200ul(10mM/DMSO) D50616 Alvelestat 1mg,2mg,200ul(10mM/DMSO) D50577 Alvimopan dihydrate 1mg,5mg D50581 Amfenac Sodium Hydrate 100mg D50653 AMG 208 2.5mg,200ul(10mM/DMSO) D50645 AMG319 2mg,5mg,100ul(10mM/DMSO) D50547 Amonafide 5mg D50614 Anacetrapib 5mg,10mg,200ul(10mM/DMSO) D50670 Anethole trithione 100mg,500mg,1ml(10mM/DMSO) D50667 Anhydroicaritin 5mg,10mg,1ml(10mM/DMSO) D52001 Anisomycin 5mg,10mg D50578 Antineoplaston A10 1mg,5mg D50530 Antipain dihydrochloride 1mg,5mg D50671 Antipyrine 10mg,50mg,1ml(10mM/DMSO) D50627 Apararenone 5mg,200ul(10mM/DMSO) D50624 Apixaban 10mg,50mg,1ml(10mM/DMSO) D10360 Aprotinin (5400 KIU/mg) 10mg,25mg,100mg D50507 Arbidol hydrochloride 10mg D50508 Arbidol Hydrochloride Hydrate 500mg D50620 ATP 5g,10g,1ml(10mM/DMSO) D50621 ATP disodium salt hydrate 1g,10g,1ml(10mM/H2O) D50635 Baicalein 100mg,1ml(10mM in DMSO) D50400 b-AP15 5mg D50400s b-AP15
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 7,893,053 B2 Seed Et Al
    US0078.93053B2 (12) United States Patent (10) Patent No.: US 7,893,053 B2 Seed et al. (45) Date of Patent: Feb. 22, 2011 (54) TREATING PSYCHOLOGICAL CONDITIONS WO WO 2006/127418 11, 2006 USING MUSCARINIC RECEPTORM ANTAGONSTS (75) Inventors: Brian Seed, Boston, MA (US); Jordan OTHER PUBLICATIONS Mechanic, Sunnyvale, CA (US) Chau et al. (Nucleus accumbens muscarinic receptors in the control of behavioral depression : Antidepressant-like effects of local M1 (73) Assignee: Theracos, Inc., Sunnyvale, CA (US) antagonist in the porSolt Swim test Neuroscience vol. 104, No. 3, pp. 791-798, 2001).* (*) Notice: Subject to any disclaimer, the term of this Lind et al. (Muscarinic acetylcholine receptor antagonists inhibit patent is extended or adjusted under 35 chick Scleral chondrocytes Investigative Ophthalmology & Visual U.S.C. 154(b) by 726 days. Science, vol.39, 2217-2231.* Chau D., et al., “Nucleus Accumbens Muscarinic Receptors in the (21) Appl. No.: 11/763,145 Control of Behavioral Depression: Antidepressant-like Effects of Local M1 Antagonists in the Porsolt Swin Test.” Neuroscience, vol. (22) Filed: Jun. 14, 2007 104, No. 3, Jun. 14, 2001, pp. 791-798. Bechtel, W.D., et al., “Biochemical pharmacology of pirenzepine. (65) Prior Publication Data Similarities with tricyclic antidepressants in antimuscarinic effects only.” Arzneimittelforschung, vol. 36(5), pp. 793-796 (May 1986). US 2007/O293480 A1 Dec. 20, 2007 Chau, D.T. et al., “Nucleus accumbens muscarinic receptors in the control of behavioral depression: antidepressant-like effects of local Related U.S. Application Data Mantagonist in the Porsolt Swim test.” Neuroscience, vol. 104(3), (60) Provisional application No.
    [Show full text]
  • Davey KJ Phd 2013.Pdf
    UCC Library and UCC researchers have made this item openly available. Please let us know how this has helped you. Thanks! Title The gut microbiota as a contributing factor to antipsychotic-induced weight gain and metabolic dysfunction Author(s) Davey, Kieran Publication date 2013 Original citation Davey, K. 2013. The gut microbiota as a contributing factor to antipsychotic-induced weight gain and metabolic dysfunction. PhD Thesis, University College Cork. Type of publication Doctoral thesis Rights © 2013. Kieran Davey http://creativecommons.org/licenses/by-nc-nd/3.0/ Embargo information Restricted to everyone for one year Item downloaded http://hdl.handle.net/10468/1243 from Downloaded on 2021-10-09T20:00:22Z Ollscoil na hEireann National Unversity Ireland Colaiste na hOllscoile, Corcaigh University College Cork School of Pharmacy The Gut Microbiota as a Contributing Factor to Antipsychotic-Induced Weight Gain and Metabolic Dysfunction Thesis presented by Kieran J. Davey under the supervision of Prof. John F. Cryan Prof. Timothy G. Dinan Dr Siobhain M. O’Mahony for the degree of Doctor of Philosophy Head of School: CatrionaO’Driscoll Contents Declaration ........................................................................................................................................... vii Acknowledgements .......................................................................................................................... viii Publications and presentations .....................................................................................................
    [Show full text]
  • Antipsychotics
    The Fut ure of Antipsychotic Therapy (page 7 in syllabus) Stepp,,hen M. Stahl, MD, PhD Adjunct Professor, Department of Psychiatry Universityyg of California, San Diego School of Medicine Honorary Visiting Senior Fellow, Cambridge University, UK Sppyonsored by the Neuroscience Education Institute Additionally sponsored by the American Society for the Advancement of Pharmacotherapy This activity is supported by an educational grant from Sunovion Pharmaceuticals Inc. Copyright © 2011 Neuroscience Education Institute. All rights reserved. Individual Disclosure Statement Faculty Editor / Presenter Stephen M. Stahl, MD, PhD, is an adjunct professor in the department of psychiatry at the University of California, San Diego School of Medicine, and an honorary visiting senior fellow at the University of Cambridge in the UK. Grant/Research: AstraZeneca, BioMarin, Dainippon Sumitomo, Dey, Forest, Genomind, Lilly, Merck, Pamlab, Pfizer, PGxHealth/Trovis, Schering-Plough, Sepracor/Sunovion, Servier, Shire, Torrent Consultant/Advisor: Advent, Alkermes, Arena, AstraZeneca, AVANIR, BioMarin, Biovail, Boehringer Ingelheim, Bristol-Myers Squibb, CeNeRx, Cypress, Dainippon Sumitomo, Dey, Forest, Genomind, Janssen, Jazz, Labopharm, Lilly, Lundbeck, Merck, Neuronetics, Novartis, Ono, Orexigen, Otsuka, Pamlab, Pfizer, PGxHealth/Trovis, Rexahn, Roche, Royalty, Schering-Plough, Servier, Shire, Solvay/Abbott, Sunovion/Sepracor, Valeant, VIVUS, Speakers Bureau: Dainippon Sumitomo, Forest, Lilly, Merck, Pamlab, Pfizer, Sepracor/Sunovion, Servier, Wyeth Copyright © 2011 Neuroscience Education Institute. All rights reserved. Learninggj Objectives • Differentiate antipsychotic drugs from each other on the basis of their pharmacological mechanisms and their associated therapeutic and side effects • Integrate novel treatment approaches into clinical practice according to best practices guidelines • Identify novel therapeutic options currently being researched for the treatment of schizophrenia Copyright © 2011 Neuroscience Education Institute.
    [Show full text]
  • Induced Obesity Xu-Feng Huang University of Wollongong, Xuzhou Medical University, [email protected]
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Research Online University of Wollongong Research Online Illawarra Health and Medical Research Institute Faculty of Science, Medicine and Health 2018 Decreased 5‐HT2cR and GHSR1a interaction in antipsychotic drug‐induced obesity Xu-Feng Huang University of Wollongong, Xuzhou Medical University, [email protected] Katrina Weston-Green University of Wollongong, [email protected] Y Yu Xuzhou Medical University, University of Wollongong Publication Details Huang, X., Weston-Green, K. & Yu, Y. (2018). Decreased 5‐HT2cR and GHSR1a interaction in antipsychotic drug‐induced obesity. Obesity Reviews, 19 (3), 396-405. Research Online is the open access institutional repository for the University of Wollongong. For further information contact the UOW Library: [email protected] Decreased 5‐HT2cR and GHSR1a interaction in antipsychotic drug‐induced obesity Abstract Second generation antipsychotics (SGAs), notably atypical antipsychotics includingolanzapine, clozapine and risperidone, can cause weight gain and obesity side ef-fects. Antagonism of serotonin 2c receptors (5-HT2cR) and activation of ghrelin re-ceptor type 1a (GHSR1a) signalling have been identified as a main cause of SGAinduced obesity. Here we review the pivotal regulatory role of the 5-HT2cR inghrelin-mediated appetite signalling. The 5-HT2cR dimerizes with GHSR1a to in-hibit orexigenic signalling, while 5-HT2cR antagonism reduces dimerization andincreases GHSR1a-induced food intake. Dimerization is specific ot the unedited5-HT2cR isoform. 5-HT2cR antagonism by SGAs may disrupt the normal inhibi-tory tone on the GHSR1a, increasing orexigenic signalling. The 5-HT2cR and itsinteraction with the GHSR1a could serve as the basis for discovering novel ap-proaches to preventing and treating SGA-induced obesity.
    [Show full text]
  • 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.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 9,365,521 B2 Blackburn Et Al
    USOO9365521B2 (12) United States Patent (10) Patent No.: US 9,365,521 B2 Blackburn et al. (45) Date of Patent: Jun. 14, 2016 (54) NON-HYGROSCOPICSALTS OF 5-HT, 5,178,786 A 1/1993 Jahnke et al. AGONSTS 5,247,080 A 9/1993 Berger et al. 5,275,915 A 1/1994 Kojima et al. 5,387,685 A 2f1995 Powell et al. (75) Inventors: Anthony C. Blackburn, San Diego, CA 5,397.793 A 3, 1995 Shaber et al. (US); Yun Shan, San Diego, CA (US); 5,412,119 A 5/1995 Brussee et al. Anna Shifrina, San Diego, CA (US); 5,422,355 A 6/1995 White et al. Scott Stirn, San Diego, CA (US) 5,691.362 A 11/1997 McCormicket al. 5,750,520 A 5/1998 Danilewicz et al. (73) Assignee: Arena Pharmaceuticals, Inc., San 5,856.5035,795,895 A 8,1/1999 1998 AnchAS al. Diego, CA (US) 5,861,393 A 1/1999 Danilewicz et al. 5,908,830 A 6/1999 Smith et al. (*) Notice: Subject to any disclaimer, the term of this 5,925,651 A 7/1999 Hutchinson patent is extended or adjusted under 35 3. A 3: As al U.S.C. 154(b) by 567 days. 5,958,943- 4 A 9/1999 Laufera etca. al. 6,087,346 A 7/2000 Glennon et al. (21) Appl. No.: 13/820,095 6,218,385 B1 4/2001 Adam et al. 6,900,313 B2 5/2005 Wasserscheid et al. (22) PCT Filed: Aug. 31, 2011 6,953,787 B2 * 10/2005 Smith .................
    [Show full text]
  • WO 2018/023009 Al 01 February 2018 (01.02.2018) W !P O PCT
    (12) INTERNATIONAL APPLICATION PUBLISHED UNDER THE PATENT COOPERATION TREATY (PCT) (19) World Intellectual Property Organization I International Bureau (10) International Publication Number (43) International Publication Date WO 2018/023009 Al 01 February 2018 (01.02.2018) W !P O PCT (51) International Patent Classification: AO, AT, AU, AZ, BA, BB, BG, BH, BN, BR, BW, BY, BZ, C07D 417/14 (2006.01) A61K 31/496 (2006.01) CA, CH, CL, CN, CO, CR, CU, CZ, DE, DJ, DK, DM, DO, A61P 25/18 (2006.01) DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, GT, HN, HR, HU, ID, IL, IN, IR, IS, JO, JP, KE, KG, KH, KN, KP, (21) International Application Number: KR, KW, KZ, LA, LC, LK, LR, LS, LU, LY, MA, MD, ME, PCT/US20 17/044400 MG, MK, MN, MW, MX, MY, MZ, NA, NG, NI, NO, NZ, (22) International Filing Date: OM, PA, PE, PG, PH, PL, PT, QA, RO, RS, RU, RW, SA, 28 July 2017 (28.07.2017) SC, SD, SE, SG, SK, SL, SM, ST, SV, SY,TH, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC, VN, ZA, ZM, ZW. (25) Filing Language: English (84) Designated States (unless otherwise indicated, for every (26) Publication Language: English kind of regional protection available): ARIPO (BW, GH, (30) Priority Data: GM, KE, LR, LS, MW, MZ, NA, RW, SD, SL, ST, SZ, TZ, 62/368,630 29 July 2016 (29.07.2016) US UG, ZM, ZW), Eurasian (AM, AZ, BY, KG, KZ, RU, TJ, TM), European (AL, AT, BE, BG, CH, CY, CZ, DE, DK, (71) Applicant: CONCERT PHARMACEUTICALS, INC.
    [Show full text]
  • The Potentially Beneficial Central Nervous System Activity Profile of Ivacaftor and Its Metabolites
    ORIGINAL ARTICLE CYSTIC FIBROSIS The potentially beneficial central nervous system activity profile of ivacaftor and its metabolites Elena K. Schneider 1,2, Rachel M. McQuade3, Vincenzo C. Carbone4, Felisa Reyes-Ortega5, John W. Wilson6,7, Brenda Button6,7, Ayame Saito3, Daniel P. Poole3, Daniel Hoyer2,8,9, Jian Li10,11 and Tony Velkov1,2,11 Affiliations: 1Drug Delivery, Disposition and Dynamics, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Australia. 2Dept of Pharmacology and Therapeutics, School of Biomedical Sciences, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Parkville, Australia. 3Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Australia. 4Animal Science, AgResearch Limited, Palmerston North, New Zealand. 5Dept of Applied Physics, Sciences Faculty, University of Granada, Granada, Spain. 6Dept of Medicine, Monash University, The Alfred Hospital, Melbourne, Australia. 7Cystic Fibrosis Service, The Alfred Hospital, Melbourne, Australia. 8The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia. 9Dept of Molecular Medicine, The Scripps Research Institute, La Jolla, CA, USA. 10Monash Biomedicine Discovery Institute, Dept of Microbiology, Monash University, Clayton, Australia. 11These two authors contributed equally to this work. Correspondence: Tony Velkov, Dept of Pharmacology and Therapeutics, The University of Melbourne, Parkville, Victoria 3010, Australia. E-mail: [email protected]
    [Show full text]
  • The Activity of the Serotonin Receptor 2C Is Regulated by Alternative Splicing Stefan Stamm University of Kentucky, [email protected]
    University of Kentucky UKnowledge Molecular and Cellular Biochemistry Faculty Molecular and Cellular Biochemistry Publications 9-2017 The Activity of the Serotonin Receptor 2C is Regulated by Alternative Splicing Stefan Stamm University of Kentucky, [email protected] Samuel B. Gruber University of Kentucky Alexander G. Rabchevsky University of Kentucky, [email protected] Ronald B. Emeson Vanderbilt University Right click to open a feedback form in a new tab to let us know how this document benefits oy u. Follow this and additional works at: https://uknowledge.uky.edu/biochem_facpub Part of the Biochemistry, Biophysics, and Structural Biology Commons, and the Genetics and Genomics Commons Repository Citation Stamm, Stefan; Gruber, Samuel B.; Rabchevsky, Alexander G.; and Emeson, Ronald B., "The Activity of the Serotonin Receptor 2C is Regulated by Alternative Splicing" (2017). Molecular and Cellular Biochemistry Faculty Publications. 160. https://uknowledge.uky.edu/biochem_facpub/160 This Article is brought to you for free and open access by the Molecular and Cellular Biochemistry at UKnowledge. It has been accepted for inclusion in Molecular and Cellular Biochemistry Faculty Publications by an authorized administrator of UKnowledge. For more information, please contact [email protected]. The Activity of the Serotonin Receptor 2C is Regulated by Alternative Splicing Notes/Citation Information Published in Human Genetics, v. 136, issue 9, p. 1079-1091. © Springer-Verlag GmbH Germany 2017 The opc yright holder has granted the permission for posting the article here. This is a post-peer-review, pre-copyedit version of an article published in Human Genetics. The final authenticated version is available online at: https://doi.org/10.1007/s00439-017-1826-3.
    [Show full text]