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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. -
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). -
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 -
(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. -
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 ..................................................................................................... -
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. -
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. -
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. -
(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 ................. -
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. -
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] -
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.