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Dextromethorphan Attenuates Sensorineural Hearing Loss in an Animal Model and Population-Based Cohort Study
International Journal of Environmental Research and Public Health Article Dextromethorphan Attenuates Sensorineural Hearing Loss in an Animal Model and Population-Based Cohort Study Hsin-Chien Chen 1,* , Chih-Hung Wang 1,2 , Wu-Chien Chien 3,4 , Chi-Hsiang Chung 3,4, Cheng-Ping Shih 1, Yi-Chun Lin 1,2, I-Hsun Li 5,6, Yuan-Yung Lin 1,2 and Chao-Yin Kuo 1 1 Department of Otolaryngology-Head and Neck Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan; [email protected] (C.-H.W.); [email protected] (C.-P.S.); [email protected] (Y.-C.L.); [email protected] (Y.-Y.L.); [email protected] (C.-Y.K.) 2 Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei 114, Taiwan 3 School of Public Health, National Defense Medical Center, Taipei 114, Taiwan; [email protected] (W.-C.C.); [email protected] (C.-H.C.) 4 Department of Medical Research, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan 5 Department of Pharmacy Practice, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan; [email protected] 6 School of Pharmacy, National Defense Medical Center, Taipei 114, Taiwan * Correspondence: [email protected]; Tel.: +886-2-8792-7192; Fax: +886-2-8792-7193 Received: 31 July 2020; Accepted: 28 August 2020; Published: 31 August 2020 Abstract: The effect of dextromethorphan (DXM) use in sensorineural hearing loss (SNHL) has not been fully examined. We conducted an animal model and nationwide retrospective matched-cohort study to explore the association between DXM use and SNHL. -
Galantamine Potentiates the Neuroprotective Effect of Memantine Against NMDA-Induced Excitotoxicity Joao~ P
Galantamine potentiates the neuroprotective effect of memantine against NMDA-induced excitotoxicity Joao~ P. Lopes1, Glauco Tarozzo1, Angelo Reggiani1, Daniele Piomelli1,2 & Andrea Cavalli1,3 1D3 – Drug Discovery and Development Department, Istituto Italiano di Tecnologia, Via Morego, 16163, Genova, Italy 2Departments of Anatomy and Neurobiology and Biological Chemistry, University of California, Irvine, CA, 92697-4621 3Department of Pharmacy and Biotechnologies, Alma Mater Studiorum, Bologna University, Via Belmeloro, 40126, Bologna, Italy Keywords Abstract Alzheimer’s disease, drug combination, N NMDA neurotoxicity, NR2B, The combination of memantine, an -methyl-D-aspartate (NMDA) receptor polypharmacology, primary cortical neurons antagonist, with an acetylcholinesterase inhibitor (AChEI) is the current stan- dard of care in Alzheimer’s disease (AD). Galantamine, an AChEI currently Correspondence marketed for the treatment of AD, exerts memory-enhancing and neuroprotec- Andrea Cavalli, D3 – Drug Discovery and tive effects via activation of nicotinic acetylcholine receptors (nAChRs). Here, Development Department, Istituto Italiano we investigated the neuroprotective properties of galantamine in primary cul- di Tecnologia – Via Morego, 30, 16163 tures of rat cortical neurons when given alone or in combination with meman- Genova, Italy. Tel: +39 010 71781530; Fax: +39 010 tine. In agreement with previous findings, we found that memantine was fully 71781228; E-mail: [email protected] effective in reversing NMDA toxicity at concentrations of 2.5 and 5 lmol/L. Galantamine also completely reversed NMDA toxicity at a concentration of Funding Information 5 lmol/L. The a7 and a4b2 nAChR antagonists, methyllycaconitine, and dihy- No funding information provided. dro-b-erythroidine blocked the neuroprotective effect of galantamine, demon- strating the involvement of nAChRs. -
Accepted Manuscript
Zurich Open Repository and Archive University of Zurich Main Library Strickhofstrasse 39 CH-8057 Zurich www.zora.uzh.ch Year: 2019 Nocturnal gamma-hydroxybutyrate reduces cortisol awakening response and morning kyrunenine pathway metabolites in healthy volunteers Dornbierer, Dario A ; Boxler, M ; Voegel, C D ; Stucky, Benjamin ; Steuer, A E ; Binz, T M ; Baumgartner, M R ; Baur, Diego M ; Quednow, B B ; Kraemer, T ; Seifritz, E ; Landolt, Hans-Peter ; Bosch, O G Abstract: Background Gamma-hydroxybutyrate (GHB; or sodium oxybate) is an endogenous GHB- /GABAB receptor agonist. It is approved for the application in narcolepsy and has been proposed for potential treatment of Alzheimer’s and Parkinson’s disease, fibromyalgia, and depression, all of which involve neuro-immunological processes. Tryptophan catabolites (TRYCATs), the cortisol awakening re- sponse (CAR), and brain derived neurotrophic factor (BDNF) have been suggested as peripheral biomark- ers of neuropsychiatric disorders. GHB has been shown to induce a delayed reduction of T helper and natural killer cell counts and alter basal cortisol levels, but GHB’s effects on TRYCATs, CAR and BDNF are unknown. Methods Therefore, TRYCAT and BDNF serum levels as well as CAR and the affec- tive state (Positive and Negative Affect Schedule, PANAS) were measured in the morning after asingle nocturnal dose of GHB (50 mg/kg body weight) in 20 healthy male volunteers in a placebo-controlled, balanced, randomized, double-blind, cross-over design. Results In the morning after nocturnal GHB administration, the TRYCATs indolelactic acid, kynurenine, kynurenic acid, 3-hydroxykynurenine, and quinolinic acid, the 3-hydroxykynurenine to kynurenic acid ratio and the CAR were significantly re- duced (p<0.05-0.001, Benjamini-Hochberg corrected). -
Both N-Methyl-D-Aspartate and Non-N-Methyl- D-Aspartate Glutamate Receptors in the Bed
JOP0010.1177/0269881117691468Journal of PsychopharmacologyAdami et al. 691468research-article2017 Original Paper Both N-methyl-D-aspartate and non-N-methyl- D-aspartate glutamate receptors in the bed nucleus of the stria terminalis modulate the Journal of Psychopharmacology 2017, Vol. 31(6) 674 –681 cardiovascular responses to acute restraint © The Author(s) 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav stress in rats DOI:https://doi.org/10.1177/0269881117691468 10.1177/0269881117691468 journals.sagepub.com/home/jop Mariane B Adami1*, Lucas Barretto-de-Souza1,2*, Josiane O Duarte1, Jeferson Almeida1,2 and Carlos C Crestani1,2 Abstract The bed nucleus of the stria terminalis (BNST) is a forebrain structure that has been implicated on cardiovascular responses evoked by emotional stress. However, the local neurochemical mechanisms mediating the BNST control of stress responses are not fully described. In our study we investigated the involvement of glutamatergic neurotransmission within the BNST in cardiovascular changes evoked by acute restraint stress in rats. For this study, we investigated the effects of bilateral microinjections of selective antagonists of either N-methyl-D-aspartate (NMDA) or non-NMDA glutamate receptors into the BNST on the arterial pressure and heart rate increase and the decrease in tail skin temperature induced by acute restraint stress. Microinjection of the selective NMDA glutamate receptor antagonist LY235959 (1 nmol/100 nL) into the BNST decreased the tachycardiac response to restraint stress, without affecting the arterial pressure increase and the drop in skin temperature. Bilateral BNST treatment with the selective non-NMDA glutamate receptor NBQX (1 nmol/100 nL) decreased the heart rate increase and the fall in tail skin temperature, without affecting the blood pressure increase. -
The Effects of Dextromethorphan on Response Acquisition with Delayed Reinforcement
Western Michigan University ScholarWorks at WMU Dissertations Graduate College 6-2005 The Effects of Dextromethorphan on Response Acquisition with Delayed Reinforcement Thomas B. Morgan Western Michigan University Follow this and additional works at: https://scholarworks.wmich.edu/dissertations Part of the Mental and Social Health Commons, and the Psychology Commons Recommended Citation Morgan, Thomas B., "The Effects of Dextromethorphan on Response Acquisition with Delayed Reinforcement" (2005). Dissertations. 1050. https://scholarworks.wmich.edu/dissertations/1050 This Dissertation-Open Access is brought to you for free and open access by the Graduate College at ScholarWorks at WMU. It has been accepted for inclusion in Dissertations by an authorized administrator of ScholarWorks at WMU. For more information, please contact [email protected]. THE EFFECTS OF DEXTROMETHORPHAN ON RESPONSE ACQUISITION WITH DELAYED REINFORCEMENT by Thomas B. Morgan A Dissertation Submitted to the Faculty of The Graduate College in partial fulfillment of the requirements for the Degree of Doctor of Philosophy Department of Psychology Western Michigan University Kalamazoo, Michigan June 2005 THE EFFECTS OF DEXTROMETHORPHAN ON RESPONSE ACQUISITION WITH DELAYED REINFORCEMENT Thomas B. Morgan, Ph. D. Western Michigan University, 2005 The current study examined in 2-h sessions the effects of intraperitoneal injec- tions of dextromethorphan (DM) (0.0, 40.0, 60.0, and 80.0 mg/kg) on the acquisition of lever-press responding in rats that were exposed to a two-lever procedure in which responses on the reinforcement lever (RL) were reinforced with food after a 15-s re- setting delay and responses on the cancellation lever cancelled a scheduled reinforcer. -
A Steroid Modulatory Domain on NR2B Controls N-Methyl-D-Aspartate Receptor Proton Sensitivity
A steroid modulatory domain on NR2B controls N-methyl-D-aspartate receptor proton sensitivity Ming-Kuei Jang†, Dale F. Mierke‡, Shelley J. Russek†, and David H. Farb†§ †Laboratory of Molecular Neurobiology, Department of Pharmacology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118; and ‡Department of Molecular Pharmacology, Division of Biology and Medicine, and Department of Chemistry, Brown University, Providence, RI 02912 Edited by Erminio Costa, University of Illinois, Chicago, IL, and approved April 5, 2004 (received for review March 15, 2004) N-methyl-D-aspartate (NMDA) receptor function is modulated by have been shown to regulate native NMDA receptors via distinct several endogenous molecules, including zinc, polyamines, pro- recognition sites; PS modulation is also not dependent on the tons, and sulfated neurosteroids. Zinc, polyamines, and phenyleth- redox state of the receptor (24). To define the mode of action of anolamines exert their respective modulatory effects by exacer- PS and to determine structural components at the NMDA bating or relieving tonic proton inhibition. Here, we report that receptor that are critical for PS modulation, we took advantage pregnenolone sulfate (PS) uses a unique mechanism for enhance- of our previous finding that PS differentially modulates activity ment of NMDA receptor function that is independent of the proton of recombinant receptors containing different NR2 subunits sensor. We identify a steroid modulatory domain, SMD1, on the (25). PS potentiates the response of recombinant NMDA re- NMDA receptor NR2B subunit that is critical for both PS enhance- ceptors containing NR2A or NR2B subunits, while inhibiting the ment and proton sensitivity. This domain includes the J͞K helices response of receptors containing NR2C or NR2D subunits. -
(200731) Hypromellose Phthalate (220824) Ibudilast
21222122 Infrared Reference Spectra JP XVII Hypromellose Phthalate (200731) Hypromellose Phthalate (220824) Ibudilast The JP Drugs are to be tested according to the provisions given in the pertinent monographs, General Notices, General Rules for Crude Drugs, General Rules for Preparations, and General Tests for their conformity to the Japanese Pharmacopoeia. (See the General Notices 5.) JP XVII Infrared Reference Spectra 21232123 Ibuprofen Ibuprofen Piconol Ifenprodil Tartrate The JP Drugs are to be tested according to the provisions given in the pertinent monographs, General Notices, General Rules for Crude Drugs, General Rules for Preparations, and General Tests for their conformity to the Japanese Pharmacopoeia. (See the General Notices 5.) 21242124 Infrared Reference Spectra JP XVII Imidapril Hydrochloride Imipenem Hydrate Indapamide The JP Drugs are to be tested according to the provisions given in the pertinent monographs, General Notices, General Rules for Crude Drugs, General Rules for Preparations, and General Tests for their conformity to the Japanese Pharmacopoeia. (See the General Notices 5.) JP XVII Infrared Reference Spectra 21252125 Indenolol Hydrochloride Indometacin Iohexol The JP Drugs are to be tested according to the provisions given in the pertinent monographs, General Notices, General Rules for Crude Drugs, General Rules for Preparations, and General Tests for their conformity to the Japanese Pharmacopoeia. (See the General Notices 5.) 21262126 Infrared Reference Spectra JP XVII Iopamidol Iotalamic Acid Iotroxic Acid The JP Drugs are to be tested according to the provisions given in the pertinent monographs, General Notices, General Rules for Crude Drugs, General Rules for Preparations, and General Tests for their conformity to the Japanese Pharmacopoeia. -
Thyroid Hormones Modulate GABAA Receptor-Mediated Currents in Hippocampal Neurons
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Archivio istituzionale della ricerca - Università di Modena e Reggio Emilia Neuropharmacology 60 (2011) 1254e1261 Contents lists available at ScienceDirect Neuropharmacology journal homepage: www.elsevier.com/locate/neuropharm Thyroid hormones modulate GABAA receptor-mediated currents in hippocampal neurons G. Puia*, G. Losi 1 Department of Biomedical Science, Pharmacology Section, University of Modena and Reggio Emilia, via Campi 287, 41100 Modena, Italy article info abstract Article history: Thyroid hormones (THs) play a crucial role in the maturation and functioning of mammalian central 0 Received 4 August 2010 nervous system. Thyroxine (T4) and 3, 3 ,5-L-triiodothyronine (T3) are well known for their genomic Received in revised form effects, but recently attention has been focused on their non genomic actions as modulators of neuronal 28 October 2010 activity. In the present study we report that T4 and T3 reduce, in a non competitive manner, GABA- Accepted 15 December 2010 evoked currents in rat hippocampal cultures with IC50sof13Æ 4 mM and 12 Æ 3 mM, respectively. The genomically inactive compound rev-T3 was also able to inhibit the currents elicited by GABA. Blocking Keywords: PKC or PKA activity, chelating intracellular calcium, or antagonizing the integrin receptor aVb3 with Thryoid hormones GABAergic neurotransmission TETRAC did not affect THs modulation of GABA-evoked currents. THs affect also synaptic activity in Neuronal cultures hippocampal and cortical cultured neurons. sIPSCs T3 and T4 reduced to approximately 50% the amplitude and frequency of spontaneous inhibitory Tonic currents synaptic currents (sIPSCs), without altering their decay kinetic. -
Gαq-ASSOCIATED SIGNALING PROMOTES NEUROADAPTATION to ETHANOL and WITHDRAWAL-ASSOCIATED HIPPOCAMPAL DAMAGE
University of Kentucky UKnowledge Theses and Dissertations--Psychology Psychology 2015 Gαq-ASSOCIATED SIGNALING PROMOTES NEUROADAPTATION TO ETHANOL AND WITHDRAWAL-ASSOCIATED HIPPOCAMPAL DAMAGE Anna R. Reynolds Univerity of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits ou.y Recommended Citation Reynolds, Anna R., "Gαq-ASSOCIATED SIGNALING PROMOTES NEUROADAPTATION TO ETHANOL AND WITHDRAWAL-ASSOCIATED HIPPOCAMPAL DAMAGE" (2015). Theses and Dissertations--Psychology. 74. https://uknowledge.uky.edu/psychology_etds/74 This Doctoral Dissertation is brought to you for free and open access by the Psychology at UKnowledge. It has been accepted for inclusion in Theses and Dissertations--Psychology by an authorized administrator of UKnowledge. For more information, please contact [email protected]. STUDENT AGREEMENT: I represent that my thesis or dissertation and abstract are my original work. Proper attribution has been given to all outside sources. I understand that I am solely responsible for obtaining any needed copyright permissions. I have obtained needed written permission statement(s) from the owner(s) of each third-party copyrighted matter to be included in my work, allowing electronic distribution (if such use is not permitted by the fair use doctrine) which will be submitted to UKnowledge as Additional File. I hereby grant to The University of Kentucky and its agents the irrevocable, non-exclusive, and royalty-free license to archive and make accessible my work in whole or in part in all forms of media, now or hereafter known. I agree that the document mentioned above may be made available immediately for worldwide access unless an embargo applies. -
NBQX Attenuates Excitotoxic Injury in Developing White Matter
The Journal of Neuroscience, December 15, 2000, 20(24):9235–9241 NBQX Attenuates Excitotoxic Injury in Developing White Matter Pamela L. Follett, Paul A. Rosenberg, Joseph J. Volpe, and Frances E. Jensen Department of Neurology and Program in Neuroscience, Children’s Hospital and Harvard Medical School, Boston, Massachusetts 02115 The excitatory neurotransmitter glutamate is released from axons hr) resulted in selective, subcortical white matter injury with a and glia under hypoxic/ischemic conditions. In vitro, oligoden- marked ipsilateral decrease in immature and myelin basic drocytes (OLs) express non-NMDA glutamate receptors (GluRs) protein-expressing OLs that was also significantly attenuated by and are susceptible to GluR-mediated excitotoxicity. We evalu- 6-nitro-7-sulfamoylbenzo(f)quinoxaline-2,3-dione (NBQX). Intra- ated the role of GluR-mediated OL excitotoxicity in hypoxic/ cerebral AMPA demonstrated greater susceptibility to OL injury ischemic white matter injury in the developing brain. Hypoxic/ at P7 than in younger or older pups, and this was attenuated by ischemic white matter injury is thought to mediate periventricular systemic pretreatment with the AMPA antagonist NBQX. These leukomalacia, an age-dependent white matter lesion seen in results indicate a parallel, maturation-dependent susceptibility of preterm infants and a common antecedent to cerebral palsy. immature OLs to AMPA and hypoxia/ischemia. The protective Hypoxia/ischemia in rat pups at postnatal day 7 (P7) produced efficacy of NBQX suggests a role for glutamate receptor- selective white matter lesions and OL death. Furthermore, OLs in mediated excitotoxic OL injury in immature white matter in vivo. pericallosal white matter express non-NMDA GluRs at P7. -
NIH Public Access Author Manuscript Addict Biol
NIH Public Access Author Manuscript Addict Biol. Author manuscript; available in PMC 2014 January 01. Published in final edited form as: Addict Biol. 2013 January ; 18(1): 54–65. doi:10.1111/adb.12000. Enhanced AMPA Receptor Activity Increases Operant Alcohol Self-administration and Cue-Induced Reinstatement $watermark-text $watermark-text $watermark-text Reginald Cannadya,b, Kristen R. Fishera, Brandon Duranta, Joyce Besheera,b,c, and Clyde W. Hodgea,b,c,d aBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 bCurriculum in Neurobiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 cDepartment of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 dDepartment of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599 Abstract Long-term alcohol exposure produces neuroadaptations that contribute to the progression of alcohol abuse disorders. Chronic alcohol consumption results in strengthened excitatory neurotransmission and increased AMPA receptor signaling in animal models. However, the mechanistic role of enhanced AMPA receptor activity in alcohol reinforcement and alcohol- seeking behavior remains unclear. This study examined the role of enhanced AMPA receptor function using the selective positive allosteric modulator, aniracetam, in modulating operant alcohol self-administration and cue-induced reinstatement. Male alcohol-preferring (P-) rats, trained to self-administer alcohol (15%, v/v) versus water were pretreated with aniracetam to assess effects on maintenance of alcohol self-administration. To determine reinforcer specificity, P-rats were trained to self-administer sucrose (0.8%, w/v) versus water, and effects of aniracetam were tested. -
Mapping the Binding Site of the Neuroprotectant Ifenprodil on NMDA Receptors
The Journal of Neuroscience, July 15, 2002, 22(14):5955–5965 Mapping the Binding Site of the Neuroprotectant Ifenprodil on NMDA Receptors Florent Perin-Dureau, Julie Rachline, Jacques Neyton, and Pierre Paoletti Laboratoire de Neurobiologie, Centre National de la Recherche Scientifique, Unite´ Mixte de Recherche 8544, Ecole Normale Supe´ rieure, 75005 Paris, France Ifenprodil is a noncompetitive antagonist of NMDA receptors control ifenprodil inhibition. Their location in a modeled three- highly selective for the NMDA receptor 2B (NR2B) subunit. It is dimensional structure suggests that ifenprodil binds in the cleft widely used as a pharmacological tool to discriminate sub- of the LIVBP-like domain of NR2B by a mechanism (Venus- populations of NMDA receptors, and derivatives are currently flytrap) resembling that of the binding of Zn on the LIVBP-like being developed as candidate neuroprotectants. Despite nu- domain of NR2A. These results reinforce the proposal that the merous studies on the mechanism of action of ifenprodil on LIVBP-like domains of NMDA receptors, and possibly of other NMDA receptors, the structural determinants responsible for ionotropic glutamate receptors, bind modulatory ligands. More- the subunit selectivity have not been identified. By combining over, they identify the LIVBP-like domain of the NR2B subunit functional studies on recombinant NMDA receptors and bio- as a promising therapeutic target and provide a framework for chemical studies on isolated domains, we now show that ifen- designing structurally novel NR2B-selective