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Mglu2 Receptor Agonism, but Not Positive Allosteric Modulation, Elicits Rapid Tolerance Towards Their Primary Efficacy on Sleep Measures in Rats
RESEARCH ARTICLE mGlu2 Receptor Agonism, but Not Positive Allosteric Modulation, Elicits Rapid Tolerance towards Their Primary Efficacy on Sleep Measures in Rats Abdallah Ahnaou1*, Hilde Lavreysen1, Gary Tresadern2, Jose M. Cid2, Wilhelmus H. Drinkenburg1 1 Dept. of Neuroscience, Janssen Research & Development, A Division of Janssen Pharmaceutica N.V., Turnhoutseweg 30, B-2340, Beerse, Belgium, 2 Neuroscience Medicinal Chemistry, Janssen Research & Development, Janssen-Cilag S.A., Jarama 75, Polígono Industrial, 45007, Toledo, Spain * [email protected] Abstract OPEN ACCESS G-protein-coupled receptor (GPCR) agonists are known to induce both cellular adaptations Citation: Ahnaou A, Lavreysen H, Tresadern G, Cid resulting in tolerance to therapeutic effects and withdrawal symptoms upon treatment dis- JM, Drinkenburg WH (2015) mGlu2 Receptor continuation. Glutamate neurotransmission is an integral part of sleep-wake mechanisms, Agonism, but Not Positive Allosteric Modulation, Elicits Rapid Tolerance towards Their Primary which processes have translational relevance for central activity and target engagement. Efficacy on Sleep Measures in Rats. PLoS ONE 10 Here, we investigated the efficacy and tolerance potential of the metabotropic glutamate (12): e0144017. doi:10.1371/journal.pone.0144017 receptors (mGluR2/3) agonist LY354740 versus mGluR2 positive allosteric modulator Editor: James Porter, University of North Dakota, (PAM) JNJ-42153605 on sleep-wake organisation in rats. In vitro, the selectivity and UNITED STATES potency of JNJ-42153605 were characterized. In vivo, effects on sleep measures were Received: July 12, 2015 investigated in rats after once daily oral repeated treatment for 7 days, withdrawal and con- Accepted: November 12, 2015 secutive re-administration of LY354740 (1–10 mg/kg) and JNJ-42153605 (3–30 mg/kg). -
Examples of Successful Protein Expression with SUMO Reference Protein Type Family Kda System (Pubmed ID)
Examples of Successful Protein Expression with SUMO Reference Protein Type Family kDa System (PubMed ID) 23 (FGF23), human Growth factor FGF superfamily ~26 E. coli 22249723 SARS coronavirus (SARS-CoV) membrane 3C-like (3CL) protease Viral membrane protein protein 33.8 E. coli 16211506 5′nucleotidase-related apyrase (5′Nuc) Saliva protein (apyrase) 5′nucleotidase-related proteins 65 E. coli 20351782 Acetyl-CoA carboxylase 1 (ACC1) Cytosolic enzyme Family of five biotin-dependent carboxylases ~7 E. coli 22123817 Acetyl-CoA carboxylase 2 (ACC2) BCCP domain Cytosolic enzyme Family of five biotin-dependent carboxylases ~7 E. coli 22123817 Actinohivin (AH) Lectin Anti-HIV lectin of CBM family 13 12.5 E. coli DTIC Allium sativum leaf agglutinin (ASAL) Sugar-binding protein Mannose-binding lectins 25 E. coli 20100526 Extracellular matrix Anosmin protein Marix protein 100 Mammalian 22898776 Antibacterial peptide CM4 (ABP-CM4) Antibacterial peptide Cecropin family of antimicrobial peptides 3.8 E. coli 19582446 peptide from centipede venoms of Scolopendra Antimicrobial peptide scolopin 1 (AMP-scolopin 1) small cationic peptide subspinipes mutilans 2.6 E. coli 24145284 Antitumor-analgesic Antitumor-analgesic peptide (AGAP) peptide Multifunction scorpion peptide 7 E. coli 20945481 Anti-VEGF165 single-chain variable fragment (scFv) Antibody Small antibody-engineered antibody 30 E. coli 18795288 APRIL TNF receptor ligand tumor necrosis factor (TNF) ligand 16 E. coli 24412409 APRIL (A proliferation-inducing ligand, also named TALL- Type II transmembrane 2, TRDL-1 and TNFSF-13a) protein Tumor necrosis factor (TNF) family 27.51 E. coli 22387304 Aprotinin/Basic pancreatic trypsin inhibitor (BPTI) Inhibitor Kunitz-type inhibitor 6.5 E. -
Physiological and Pharmacological Characteristics of Quisqualic Acid-Induced K؉-Current Response in the Ganglion Cells of Aplysia
Japanese Journal of Physiology, 51, 511–521, 2001 Physiological and Pharmacological Characteristics of Quisqualic Acid-Induced K1-Current Response in the Ganglion Cells of Aplysia Shingo KIMURA, Satoshi KAWASAKI, Koichiro TAKASHIMA, and Kazuhiko SASAKI Department of Physiology and Advanced Medical Science Research Center, School of Medicine, Iwate Medical University, Morioka, 020–8505 Japan Abstract: The extracellular application of ei- the application of either kainate or AMPA, ago- ther quisqualic acid (QA) or Phe-Met-Arg-Phe- nists for non-NMDA receptors, produced no type NH2 (FMRFamide) induces an outward current in of response in the same neurons. The QA-in- identified neurons of Aplysia ganglion under volt- duced K1-current response was not depressed age clamp. The time course of the QA-induced at all by an intracellular injection of either gua- response is significantly slower than that induced nosine 59-O-(2-thiodiphosphate) (GDP-bS) or by FMRFamide. The reversal potential for both guanosine 59-O-(3-thiotriphosphate) (GTP-gS), responses was 292 mV and was shifted 17 mV but the FMRFamide-induced response was in a positive direction for a twofold increase in markedly blocked by both GDP-bS and GTP-gS the extracellular K1 concentration. The QA-in- in the same cell. Furthermore, the QA- and FMR- duced response was markedly depressed in the Famide-induced K1-current responses were both presence of Ba21, a blocker of inward rectifier decreased markedly when the temperature was K1-channel, whereas TEA, a Ca21-activated K1- lowered to 15°C, from 23°C. These results sug- 1 1 channel (BKCa) blocker, or 4-AP, a transient K gested that the QA-induced K -current response (A)-channel blocker, had no effect on the re- is produced by an activation of a novel type of sponse. -
Download Product Insert (PDF)
Product Information CNQX Item No. 14618 CAS Registry No.: 115066-14-3 Formal Name: 1,2,3,4-tetrahydro-7-nitro-2,3-dioxo-6- quinoxalinecarbonitrile H Synonyms: 6-cyano-7-Nitroquinoxaline-2,3-dione, NC N O FG 9065 MF: C9H4N4O4 FW: 232.2 O O N N Purity: ≥98% 2 Stability: ≥2 years at -20°C H Supplied as: A crystalline solid λ UV/Vis.: max: 217, 275, 315 nm Laboratory Procedures For long term storage, we suggest that CNQX be stored as supplied at -20°C. It should be stable for at least two years. CNQX is supplied as a crystalline solid. A stock solution may be made by dissolving the CNQX in the solvent of choice. CNQX is soluble in organic solvents such as DMSO and dimethyl formamide (DMF), which should be purged with an inert gas. The solubility of CNQX in these solvents is approximately 5 and 12 mg/ml, respectively. CNQX is sparingly soluble in aqueous buffers. For maximum solubility in aqueous buffers, CNQX should first be dissolved in DMF and then diluted with the aqueous buffer of choice. CNQX has a solubility of approximately 0.5 mg/ml in a 1:1 solution of DMF:PBS (pH 7.2) using this method. We do not recommend storing the aqueous solution for more than one day. CNQX is a competitive, non-NMDA glutamate receptor antagonist (IC50s = 0.3 and 1.5 μM for AMPA and kainate 1,2 receptors, respectively, versus IC50 = 25 μM for NMDA receptors). This compound has been used to specifically target AMPA and kainate receptor responses and thus differentiate from that of NMDA receptors. -
Selective Blockade of the Metabotropic Glutamate Receptor Mglur5 Protects Mouse Livers in in Vitro and Ex Vivo Models of Ischemia Reperfusion Injury
International Journal of Molecular Sciences Article Selective Blockade of the Metabotropic Glutamate Receptor mGluR5 Protects Mouse Livers in In Vitro and Ex Vivo Models of Ischemia Reperfusion Injury Andrea Ferrigno 1,* ID , Clarissa Berardo 1, Laura Giuseppina Di Pasqua 1, Veronica Siciliano 1, Plinio Richelmi 1, Ferdinando Nicoletti 2,3 and Mariapia Vairetti 1 ID 1 Department of Internal Medicine and Therapeutics, Cellular and Molecular Pharmacology and Toxicology Unit, University of Pavia, 27100 Pavia, Italy; [email protected] (C.B.); [email protected] (L.G.D.P.); [email protected] (V.S.); [email protected] (P.R.); [email protected] (M.V.) 2 Department of Physiology and Pharmacology, Sapienza University, 00185 Roma, Italy; [email protected] 3 I.R.C.C.S. Neuromed, 86077 Pozzilli, Italy * Correspondence: [email protected]; Tel.: +39-0382-986451 Received: 20 November 2017; Accepted: 22 January 2018; Published: 23 January 2018 Abstract: 2-Methyl-6-(phenylethynyl)pyridine (MPEP), a negative allosteric modulator of the metabotropic glutamate receptor (mGluR) 5, protects hepatocytes from ischemic injury. In astrocytes and microglia, MPEP depletes ATP. These findings seem to be self-contradictory, since ATP depletion is a fundamental stressor in ischemia. This study attempted to reconstruct the mechanism of MPEP-mediated ATP depletion and the consequences of ATP depletion on protection against ischemic injury. We compared the effects of MPEP and other mGluR5 negative modulators on ATP concentration when measured in rat hepatocytes and acellular solutions. We also evaluated the effects of mGluR5 blockade on viability in rat hepatocytes exposed to hypoxia. Furthermore, we studied the effects of MPEP treatment on mouse livers subjected to cold ischemia and warm ischemia reperfusion. -
Metabotropic Glutamate Receptors
mGluR Metabotropic glutamate receptors mGluR (metabotropic glutamate receptor) is a type of glutamate receptor that are active through an indirect metabotropic process. They are members of thegroup C family of G-protein-coupled receptors, or GPCRs. Like all glutamate receptors, mGluRs bind with glutamate, an amino acid that functions as an excitatoryneurotransmitter. The mGluRs perform a variety of functions in the central and peripheral nervous systems: mGluRs are involved in learning, memory, anxiety, and the perception of pain. mGluRs are found in pre- and postsynaptic neurons in synapses of the hippocampus, cerebellum, and the cerebral cortex, as well as other parts of the brain and in peripheral tissues. Eight different types of mGluRs, labeled mGluR1 to mGluR8, are divided into groups I, II, and III. Receptor types are grouped based on receptor structure and physiological activity. www.MedChemExpress.com 1 mGluR Agonists, Antagonists, Inhibitors, Modulators & Activators (-)-Camphoric acid (1R,2S)-VU0155041 Cat. No.: HY-122808 Cat. No.: HY-14417A (-)-Camphoric acid is the less active enantiomer (1R,2S)-VU0155041, Cis regioisomer of VU0155041, is of Camphoric acid. Camphoric acid stimulates a partial mGluR4 agonist with an EC50 of 2.35 osteoblast differentiation and induces μM. glutamate receptor expression. Camphoric acid also significantly induced the activation of NF-κB and AP-1. Purity: ≥98.0% Purity: ≥98.0% Clinical Data: No Development Reported Clinical Data: No Development Reported Size: 10 mM × 1 mL, 100 mg Size: 10 mM × 1 mL, 5 mg, 10 mg, 25 mg (2R,4R)-APDC (R)-ADX-47273 Cat. No.: HY-102091 Cat. No.: HY-13058B (2R,4R)-APDC is a selective group II metabotropic (R)-ADX-47273 is a potent mGluR5 positive glutamate receptors (mGluRs) agonist. -
An Investigation Into Pro-Apoptotic Targets in Experimental Glaucoma and the Neuroprotective Effects of Ginkgo Biloba in Retinal Ganglion Cells
An investigation into pro-apoptotic targets in experimental glaucoma and the neuroprotective effects of Ginkgo biloba in retinal ganglion cells Abeir Baltmr MB ChB, FRCS (Glasg) A thesis submitted to University College London for the degree of Doctor of Medicine (Research) 2012 Glaucoma and Retinal Neurodegeneration Research Group Visual Neuroscience Institute of Ophthalmology 1 Declaration I, Abeir Baltmr, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. Abeir Baltmr 2 Abstract Ginkgo biloba has been advocated as a neuroprotective agent for several years in glaucoma. In this study, immunohistochemistry was used to identify known potential molecular targets of Ginkgo biloba related to retinal ganglion cell (RGC) apoptosis in experimental glaucoma, including amyloid precursor protein (APP), Aß, cytochrome c, caspase-3 and tumor necrosis factor receptor-1 (TNF-R1). Furthermore, using apoptotic inducers related to mechanisms implicated in glaucoma, namely Dimethyl sulphoxide (DMSO), ultraviolet C (UVC) and Sodium Azide (NaN3), the effects of the terpenoid fraction of Ginkgo biloba (Ginkgolide A, Ginkgolide B and Bilobalide) were investigated separately in cultured retinal ganglion cells (RGC-5). Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay and morphological analysis of DMSO treated RGC-5 was performed using Hoechst 33342 stain. Immunohistochemistry showed a strong inverse correlation between Aß and APP in ocular hypertension (OHT) animals, with APP and Aß accumulation peaking at 1 and 12 weeks after intraocular pressure (IOP) elevation respectively. Cytochrome c and TNF-R1 expression peaked at 3 weeks, and active caspase 3 activity at 12 weeks after IOP elevation. -
Advancing Quantitative Structure Activity Relationship Strategies in Ligand-Based Computer-Aided Drug Design
ADVANCING QUANTITATIVE STRUCTURE ACTIVITY RELATIONSHIP STRATEGIES IN LIGAND-BASED COMPUTER-AIDED DRUG DESIGN By Mariusz Butkiewicz Dissertation Submitted to the Faculty of the Graduate School of Vanderbilt University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY In Chemistry August, 2014 Nashville, Tennessee Approved: Jens Meiler, Ph.D. Brian O. Bachmann, Ph.D. David W. Wright, Ph.D. Clare M. McCabe, Ph.D. Copyright © 2014 by Mariusz Butkiewicz All Rights Reserved ii DEDICATION To my parents, my sister, and Nicole. iii ACKNOWLEDGEMENTS Over the past years, I have received support and encouragement from a great number of individuals to whom I am very grateful. I would like to express my deepest and sincere gratitude to my advisor, Dr. Jens Meiler. Coming to Nashville and joining the Meiler laboratory to start my graduate studies has been a tremendous opportunity and extraordinary experience in my life. Jens was an excellent mentor and supported me on each step in my graduate career. His guidance taught me how to approach scientific problems, how to ask-the right scientific questions, and how to write and present scientific work. Jens found the right balance between encouraging my own scientific explorations and providing invaluable guidance and help. I would like to thank Dr. Meiler for making the past several years such a pleasant academic experience. The members of my dissertation committee, Dr. David Wright, Dr. Brian Bachmann, and Dr. Clare McCabe, were a great source of support and guidance for my graduate work. Their insightful comments and constructive criticism gave appreciated impulses to my research. -
Synthesis and Biological Evaluation
Margarida Leonor Florindo Espadinha Licenciatura em Química Aplicada Enantiopure bicyclic lactams: synthesis and biological evaluation Dissertação para obtenção do Grau de Mestre em Química Bioorgânica Orientador: Prof. Doutora Maria M. M. Santos, FF-UL Elemento de Ligação: Prof. Doutora Paula Sério Branco, FCT-UNL Presidente: Prof. Doutora Paula Sério Branco, FCT-UNL Arguente: Prof. Doutor Vasco Bonifácio, IST-CQFM Vogal: Prof. Doutora Maria M. M. Santos, FF-UL Outubro 2015 i LOMBADA biological evaluation biological dinha synthesis and and synthesis : Margarida Espa Margarida lactams bicyclic Enantiopure ii 2015 Margarida Leonor Florindo Espadinha Licenciatura em Química Aplicada Enantiopure bicyclic lactams: synthesis and biological evaluation Dissertação para obtenção do Grau de Mestre em Química Bioorgânica Orientador: Prof. Doutora Maria M. M. Santos, FF-UL Elemento de Ligação: Prof. Doutora Paula Sério Branco, FCT Presidente: Prof. Doutora Paula Sério Branco, FCT-UNL Arguente: Doutor Vasco Bonifácio, IST-CQFM Vogal: Prof. Doutora Maria M. M. Santos, FF-UL Outubro 2015 iii Enantiopure bicyclic lactams: synthesis and biological evaluation Margarida Leonor Florindo Espadinha, Copyright A Faculdade de Ciências e Tecnologia e a Universidade Nova de Lisboa têm o direito, perpétuo e sem limites geográficos, de arquivar e publicar esta dissertação através de exemplares impressos reproduzidos em papel ou de forma digital, ou por outro qualquer meio conhecido ou que venha a ser inventado e de divulgar através de repositórios científicos e de admitir a sua cópia e distribuição com objectivos educacionais ou de investigação, não comerciais, desde que seja dado crédito ao autor e editor. iv Acknowledgements I would like to thank Professor Dr. Maria M. -
Animal Venom Derived Toxins Are Novel Analgesics for Treatment Of
Short Communication iMedPub Journals 2018 www.imedpub.com Journal of Molecular Sciences Vol.2 No.1:6 Animal Venom Derived Toxins are Novel Upadhyay RK* Analgesics for Treatment of Arthritis Department of Zoology, DDU Gorakhpur University, Gorakhpur, UP, India Abstract *Corresponding authors: Ravi Kant Upadhyay Present review article explains use of animal venom derived toxins as analgesics of the treatment of chronic pain and inflammation occurs in arthritis. It is a [email protected] progressive degenerative joint disease that put major impact on joint function and quality of life. Patients face prolonged inappropriate inflammatory responses and bone erosion. Longer persistent chronic pain is a complex and debilitating Department of Zoology, DDU Gorakhpur condition associated with a large personal, mental, physical and socioeconomic University, Gorakhpur, UttarPradesh, India. burden. However, for mitigation of inflammation and sever pain in joints synthetic analgesics are used to provide quick relief from pain but they impose many long Tel: 9838448495 term side effects. Venom toxins showed high affinity to voltage gated channels, and pain receptors. These are strong inhibitors of ion channels which enable them as potential therapeutic agents for the treatment of pain. Present article Citation: Upadhyay RK (2018) Animal Venom emphasizes development of a new class of analgesic agents in form of venom Derived Toxins are Novel Analgesics for derived toxins for the treatment of arthritis. Treatment of Arthritis. J Mol Sci. Vol.2 No.1:6 Keywords: Analgesics; Venom toxins; Ion channels; Channel inhibitors; Pain; Inflammation Received: February 04, 2018; Accepted: March 12, 2018; Published: March 19, 2018 Introduction such as the back, spine, and pelvis. -
Switch to Tonic Discharge by Thyrotropin-Releasing Hormone
Neuron Article Synchronized Network Oscillations in Rat Tuberoinfundibular Dopamine Neurons: Switch to Tonic Discharge by Thyrotropin-Releasing Hormone David J. Lyons,1,* Emilia Horjales-Araujo,1 and Christian Broberger1,* 1Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden *Correspondence: [email protected] (D.J.L.), [email protected] (C.B.) DOI 10.1016/j.neuron.2009.12.024 SUMMARY most common form of pituitary tumor (Burrow et al., 1981), and by the hyperprolactinaemia and sometimes galactorrhea that The pituitary hormone, prolactin, triggers lactation in is a side effect of antipsychotic drugs with DA antagonist prop- nursing mothers. Under nonlactating conditions, erties (Clemens et al., 1974; Meltzer and Fang, 1976). Yet, to prolactin secretion is suppressed by powerful inhibi- date, the cellular and network electrophysiological properties tion from hypothalamic tuberoinfundibular dopamine of the TIDA cell population have not been described. These (TIDA) neurons. Although firing pattern has been sug- factors are potentially fundamental features of prolactin regula- gested as integral to neuroendocrine control, the tion since discharge pattern may determine the functional output of neuroendocrine control of the anterior pituitary, as is observed electrical behavior of TIDA cells remains unknown. in the magnocellular system (Wakerley and Lincoln, 1973; Hatton We demonstrate that rat TIDA neurons discharge et al., 1983). Thus, the periodic bursting pattern in hypothalamic rhythmically in a robust 0.05 Hz oscillation. The oscil- gonadotropin-releasing hormone neurons is required for stimu- lation is phase locked between neurons, and while it lation of target gonadotrophs in the pituitary (Knobil, 1980). persists during chemical synaptic transmission When bursting is artificially replaced by continuous agonist stim- blockade, it is abolished by gap junction antagonists. -
A Functional Nav1.7-Navab Chimera with a Reconstituted High-Affinity Protx-II Binding Site S
Supplemental material to this article can be found at: http://molpharm.aspetjournals.org/content/suppl/2017/06/23/mol.117.108712.DC1 1521-0111/92/3/310–317$25.00 https://doi.org/10.1124/mol.117.108712 MOLECULAR PHARMACOLOGY Mol Pharmacol 92:310–317, September 2017 Copyright ª 2017 by The American Society for Pharmacology and Experimental Therapeutics A Functional NaV1.7-NaVAb Chimera with a Reconstituted High-Affinity ProTx-II Binding Site s Ramkumar Rajamani, Sophie Wu, Iyoncy Rodrigo, Mian Gao, Simon Low, Lisa Megson, David Wensel, Rick L. Pieschl, Debra J. Post-Munson, John Watson, David R. Langley, Michael K. Ahlijanian, Linda J. Bristow, and James Herrington Molecular Discovery Technologies, Wallingford, Connecticut, Princeton, New Jersey, and Waltham, Massachusetts (R.R., S.W., I.R., M.G., S.L., L.M., D.W., D.R.L.); Discovery Biology (R.L.P., D.J.P.-M., M.K.A., L.J.B., J.H.) and Lead Discovery and Optimization (J.W.), Bristol-Myers Squibb Company, Wallingford, Connecticut Downloaded from Received March 6, 2017; accepted June 14, 2017 ABSTRACT The NaV1.7 voltage-gated sodium channel is implicated in part of the voltage sensor domain 2 (VSD2) of NaV1.7. Importantly, human pain perception by genetics. Rare gain of function this chimera, DII S1–S4, forms functional sodium channels and is molpharm.aspetjournals.org mutations in NaV1.7 lead to spontaneous pain in humans whereas potently inhibited by the NaV1.7 VSD2 targeted peptide toxin loss of function mutations results in congenital insensitivity to pain. ProTx-II. Further, we show by [125I]ProTx-II binding and surface Hence, agents that specifically modulate the function of NaV1.7 plasmon resonance that the purified DII S1–S4 protein retains high have the potential to yield novel therapeutics to treat pain.