Front Matter (PDF)

Total Page:16

File Type:pdf, Size:1020Kb

Front Matter (PDF) VOLUME 265. NUMBER 3. JUNE 1993 JPETAB 265 (3) 1039-i 567 (1993) ISSN 0022-3565 1Iaak MIH W 2 5 SROOKrJAIF P1A MFn: 1’h#{149}iF The Journal of PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS A Publication of The American Society for Pharmacology and Experimental Therapeutics Founded by John J. Abel-1909 Edited for the Society by John A. Harvey Published by Williams & Wilkins COPYRIGHT © 1993 BY THE AMERICAN SOCIETY FOR PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS VIDEO TRACKERS MEASURE ANIMAL ACTIVITY Videomex-V tracks black or white images Videomex-X tracks multiple colors Can work as interfaces to IBM-PC computers )VEI1V! Columbue Multiple Zone Dietance Traveled Experiment number 4 Dietancee are in cm VIDEQMEX-V VERTICAL ACTIVITY SETUP Timee are in meconde c- Zone Map: HORIZONTAL -> ACTIVITY 3333 11111 44 333333 11111 444444 333333 11111 444444 333333 11111 444444 33333311111444444 333331111144444 3333111114444 MONITOR 33311111444 2222222222111i122222222221 22222222222111222222222222 - -- I 22222222222212222222222222 ---- 22222222222111222222222222 - -- 22222222221111122222222222 6tii1115 I - 666661111155555 -- - -- 66666611111555555 - - ------ 666666 11111 555555 GC6666 11111 555555 - - - CGGC66 11111 555555 - - --- - GGGG 11111 5555 - - VERTiCAL GG 11111 55 ACTIVITY MAZES ‘ #{231}j VIDEOMEX-V VERTICAL ACTIVITY SETUP The Videomex-V is ideal for use VIDEOMEX-V SOFTWARE FOR with mazes. It prints pattern of Now, with two (2) television WATER MAZE movement, time spent in each maze cameras, the Videomex-V can branch (area), number of visits, etc This software plots patterns of movement, measures dis- measure both Horizontal and The user can design the shape of the tance traveled and time taken by the animal to reach the goal Vertical activity. platform in a Water Maze. maze and zones using a computer mouse or Videomex-V controls. NEW! !I \ ( : vyyv i _:_ L-1i:: MULTIPLE ANIMALS IN MULTIPLE CAGES BACKGROUND MASKING & WATER STUDIES SMALL OBJECTS FILTER Now multiple animals in multiple cages The Videomex-V is ideal for can be measured according to patterns The Videomex-V provides the perfect method to measure measuring fish activity. Observa- of movement, distances traveled and primate activity behind cage bars by being able to “mask tions can be done either from a top time each animal spends in each zone out” areas not of interest to the study. The Videomex-V view, side view or both the side of their own cage. Each animal cage tracks the animal and measures distance traveled even with and top views of an aquarium. It can be partitioned into multiple zones. solid cage bars between the animal and television camera. can track a single fish or measure This is a very economical solution for New! Small objects can be eliminated making. Videomex-V insensitive to animal feces, tracking the general level of activity of a multiple cage studies. school of fish. only the largest object in the field. VIDEOMEX-X MULTI-COLOR SYSTEM The Videomex-X Multi-Color System can track up to 6 separate color markers on either animals or humans. It digitizes the image and calculates the X-Y coordinates of color marked objects 60 times per second and transfers the data in real time to an IBM-PC/AT’s hard disk. It’s ideal for tracking multiple animal activity when animals share the same space. Software is available for tracking patterns of movement, social contact, distance traveled, time spent in different zones, etc. One exceptional application for this is in human biomechanics. LAB ANIMAL RESEARCH EQUIPMENT CATALOG NOW AVAILABLE. PLEASE CONTACT US FOR MORE INFORMATION AT: COLUMBUS INSTRUMENTS INTERNATIONAL CORPORATION P.O. Box 44049 Columbus, Ohio 43204 USA PH: (614) 276-0861 FAX: (614) 276-0529 TLX: 246514 Toll Free In USA: 1-800-669-5011 The Editor of The Journal of Pharmacology and Experimental Therapeutics wishes to express appreciation to the following colleagues who acted as Guest Editors for Specific Fields in 1992. Martin W. Adler Kenneth Johnson Edson X. Albuquerque Rudolph L. Juliano Lewis Aronow David D. Ku Carl K. Buckner John S. Lazo Marie Francoise Chesselet Irwin Lucki Theodore J. Cicero Donald E. McMillan David E. Clarke Lawrence Middaugh Marlene L. Cohen William H. Morse Max Costa David L. Nelson Charles R. Craig Saul M. Schanberg Stephen K. Fisher Kenneth J. Simansky Alan Frazer Roger D. Spealman Ray W. Fuller Jack W. Strandhoy Gerald L. Gebber Boris Tabakoff Stephen G. Holtzman R. Clinton Webb E. H. Jeffrey Michael Williams Additionally, sincere thanks are due to 1060 of our colleagues not on the Editorial Advisory Board who reviewed articles for the Journal in 1992. Their contributions are acknowledged individually in the Annual Report of The Journal to The Board of Publications Trustees of The American Society for Pharmacology and Experimental Therapeutics. INDEX Volume 265, April-June, 1993 A231877, endothelium-dependent relaxa- anisms in myocytes (guinea pigs), propranobol plasma concentration tion of aorta, L- and D-enantiomers, 1527 (humans), 681 NGnitroarginine (rats), 112 Acylcarnitines, long-chain, permeability immunomodulatory effects, morphine Abe, Y., Kitada, Y. and Narimatsu, A.: Ef- and morphology, colonic mucosa (rats), 1079 fect of MCI-154, a cardiotonic agent, (rats), 955 inotropic and beta blocking effects, chi- on regional contractile function and AD-5423, haloperidol and, pharmacological meric molecule (dogs), 1105 myocardial oxygen consumption in activities, antipsychotic efficacy and/ beta-i, mechanism of action, denopamine the presence and absence of coronary or adverse side effects (rats), 745 (rabbits), 1292 artery stenosis in dogs, 819 Adenine, pharmacological characterization beta-i and beta-2, desensitization, lipo- Abreu, M. E., see Clissold, D. B., 876 of N-0840, 227 lytic responses of adipocytes (ham- Abreu, M. E., see Karbon, E. W., 866 Adenosine sterS), 237 Absence, precipitated agonists, ventilation effects (monkeys), beta-2, independent relaxation in aorta, chronic diazepam (dogs), 1152 971 tyramine (rats), 1096 concentration-response curves, opiate-dc- Al-selective agonist RG14202 (pigs), 699 beta prejunctional, modulation of sympa- pendent ileum (guinea pigs), 1519 effects of lemakalim, comparison of vaso- thetic neurotransmission, mesentery Acetylcholine dilators (dogs), 1026 (rats), 657 cholinergic interaction, atpha-2 adreno- metabolite, inhibition, proliferation of comparison of vasodilators, lemakalim ceptor-mediated antinociception nontransformed cells (mice), 790 (dogs), 1026 (sheep), 536 Adenosine triphosphatase, inhibitors, inhi- contractile responses in vas deferens, effects of lemakalim, comparison of vaso- bition of relaxation, nitroglycerin atrial natriuretic peptide, inhibition dilators (dogs), 1026 and atrial natriuretic factor (rabbits), of purinergic component (guinea endothelium-dependent relaxation of 1187 pigs), 920 aorta, L- and D-enantiomers, N’-ni- Adenosine triphosphate pharmacokinetics and pharmacody- tro-arginine (rats), 112 P2 purinergic receptors namics, normal children and adoles- extracellular human breast tumor cells, 1499 cents, 1232 increased levels, sigma ligands in fron- pharmacological characterization, re- Adrenochrome, implication of oxygen radi- tal cortex (rats), 851 novasculature (rats), 334 cals, metabolism of cycbosporine A microdialysis, 1,2,3,4-tetrahydro-9- -sensitive potassium channel and FK-506, liver microsomes (rats, aminoacridine, striatum (rats), 759 action potential durations, minoxidil humans), 1047 pharmacological characterization, reno- sulfate-induced shortening (guinea Aging, stereoselective pharmacokinetics and vascular P2 purinergic receptors pigs), 1527 pharmacodynamics, verapamil (hu- (rats), 334 blocker glyburide, natriuretic proper- mans), 690 receptors and nicotinic binding sites, ties (rats), 933 Ahmed, S. S., Strobe!, H. W., Napoli, K. L. neuroblastoma clone line (humans), cardioprotection with zofenopril, myo- and Grevel, J.: Adrenochrome reac- 294 cardial ischemia (rats), 609 tion implicates oxygen radicals in responses of circular myometrium, pro- no abolishment of preconditioning, is- metabolism of cyclosporine A and gesterone and mifepristone, oxytocin chemic heart (rats), 559 FK-506 in rat and human liver mi- (rats), 1205 relaxation of coronary arteries, calci- crosomes, 1047 N-Acetylcysteine, inhibition of angiotensin tonin gene-related peptide (pigs), 490 AIDS, gastrointestinal and hepatic first- converting enzyme (rats), 1239 Adenylate cyclase, short-term desensitiza- pass elimination, 2’,3’-dideoxyino- N-Acetyl fl-endorphin(1-31), substance P tion, muscarinic m2 receptors, cere- sine (rats), 731 and, supraspinal antinociception, mu bellar granule cells (rats), 433 Airway, smooth muscle, functional role, opioid and alpha-2 adrenoceptors Adipocytes, lipolytic responses, desensiti- phosphodiesterase isozymes (hu- (mice), 835 zation, beta-i and beta-2 adrenocep- mans), 1213 N-Acetyl-neurotensin(8-13), inhibition of tors (hamsters), 237 Akaike, A., see Tamura, Y., 1017 vascular leakage, tissue injury (rats), Adrenal gland, pharmacological character- Albuquerque, E. X., see Alkondon, M., 1455 619 ization, SR 47436 (rats, dogs, mon- Albuquerque, E. X., see Pereira, E. F. R., Acetylsalicylic acid, airway smooth muscle keys), 826 1474 function during development, Bay K Adrenoceptors Albuquerque, M. L., see Kurth, C. D., 587 8644 and CGP 28392 (guinea pigs), alpha, functional characterization, intra- Aldershvile, J., see Boesgaard, S., 1239 524 renal arteries (rabbits), 807 Aldrich, P. E., see Wong, P. C., 1088 Acid, secretion
Recommended publications
  • Grayanotoxin Poisoning in Humans from Honey Consumption HELENA COLOMA DÍEZ AUTONOMOUS UNIVERSITY of BARCELONA
    Grayanotoxin Poisoning in Humans from Honey Consumption HELENA COLOMA DÍEZ AUTONOMOUS UNIVERSITY OF BARCELONA Objectives Structure, Types and Isolation of GTX The main objective of this bibliographic research is compiling and announcing information Grayanotoxins are non-volatile diterpenes, a about grayanotoxin-containing honey and the toxic effects derived from its ingestion. This polyhidroxylated cyclic hydrocarbon with a 5/7/6/5 ring substance is believed to have medicinal properties, and the current increment of use of structure that does not contain nitrogen, as seen on figure 2. There are 25 known isoforms of grayanotoxins, natural products as dietetic complements with this finality may cause a rising in the number GTX-I and GTX-III being the most common and of intoxication cases. So it is important learning to recognise the clinical signs it causes and abundant ones, followed by GTX-II. their treatment, apart from finding out if it may have medicinal applications. TheGTXcanbeisolatedbytypicalextraction procedures for naturally occurring terpenes, such as paper electrophoresis, thin-layer chromatography (TLC), and gas chromatography (GC). They require derivatization before GC analysis due to the Introduction compound’s instability on heating and having low vapor pressure. Other identification techniques are based on The poisoning caused by grayanotoxin-containing honey, called “mad honey”, is known from infrared (IR), nuclear magnetic resonance (NMR), and antiquity. This toxic honey has been used for different purposes, such as biological weapon mass spectrometry (MS). or therapeutical product. Figure 2. Structure formulas (left pannel) and 3D The origin of this toxin relays in some plants of the Rhododendron genus, widespread all representations (right pannel) of GTX-I, II and III.
    [Show full text]
  • Mad Honey Poisoning: a Review Rakesh Gami1* and Prajwal Dhakal2 1All Saints University, St
    linica f C l To o x l ic a o n r l o u g o y J Gami and Dhakal, J Clin Toxicol 2017, 7:1 Journal of Clinical Toxicology DOI: 10.4172/2161-0495.1000336 ISSN: 2161-0495 Review article Open Access Mad Honey Poisoning: A Review Rakesh Gami1* and Prajwal Dhakal2 1All Saints University, St. Vincent and The Grenadines 2Michigan State University, East Lansing, MI, USA *Corresponding author: Rakesh Gami, Assistant Professor, Department of Epidemiology, College of Medicine, All Saints University, St. Vincent and The Grenadines, Tel: +1-443-854-8522; E-mail: [email protected] Received date: January 01, 2017, Accepted date: January 19, 2017; Published date: January 20, 2017 Copyright: © 2017 Gami R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Mad honey, which is different from normal commercial honey, is contaminated with grayanotoxins and causes intoxication. It is used as an alternative therapy for hypertension, peptic ulcer disease and is also being used more commonly for its aphrodisiac effects. Grayanotoxins, found in rhododendron plant, act on sodium ion channels and place them in partially open state. They also act on muscarinic receptors. Cardiac manifestations of mad honey poisoning include hypotension and rhythm disorders such as bradycardia, nodal rhythm, atrial fibrillation, complete atrioventricular block or even complete heart block. Additionally, patients may develop dizziness, nausea and vomiting, weakness, sweating, blurred vision, diplopia and impaired consciousness.
    [Show full text]
  • Medical Marijuana… Fact Versus Fiction
    MEDICAL MARIJUANA… FACT VERSUS FICTION Thomas F. Jan, DO, FAOCPMR Subspecialty Certified– Pain Medicine Diplomate – American Board of Addiction Medicine MASSAPEQUA PAIN MANAGEMENT AND REHABILITATION ADMINISTRATIVE DIRECTOR-CHRONIC PAIN MANAGEMENT 4200 SUNRISE HIGHWAY MATHER HOSPITAL-NORTHWELL HEALTH MASSAPEQUA, NY 11758 PORT JEFFERSON, NY 516-541-1064 THE I LOVE ME SLIDE: THOMAS F. JAN, DO, FAOCPMR, FKIA • 20 years private practice, board certified in pain medicine and addiction medicine • Current Chair, American Osteopathic Pain Medicine Conjoint Exam Committee • Administrative Director for Chronic Pain Management, John T. Mather Hospital, Port Jefferson, NY • Core faculty, PM&R residency program, Mercy Medical Center, Catholic Health System • Leadership Council, Long Island Council on Alcoholism and Drug Dependence (LICADD) • Medical Director, LICADD Opioid Overdose Prevention Program • Member, Nassau County, NY, County Executive's task force on Heroin and Prescription drug abuse • Former Medical Director, Town of Babylon Drug and Alcohol Program Disclosures: Speaker Bureau, US WorldMeds, Lucemyra OBJECTIVES A brief history of marijuana and its medical uses throughout history How does one get certified to prescribe medical marijuana Discussion about the endocannabinoid system (ECS) What receptors are there and what are they purported to do How do the various options affect the body through the ECS What are the risks involved and some discussion about the science MEDICAL MARIJUANA FOR OPIATE ADDICTION “I prescribed the cannabis simply
    [Show full text]
  • Interaction of Batrachotoxin with the Local Anesthetic Receptor Site in Transmembrane Segment IVS6 of the Voltage-Gated Sodium Channel
    Proc. Natl. Acad. Sci. USA Vol. 95, pp. 13947–13952, November 1998 Pharmacology Interaction of batrachotoxin with the local anesthetic receptor site in transmembrane segment IVS6 of the voltage-gated sodium channel NANCY J. LINFORD,ANGELA R. CANTRELL,YUSHENG QU,TODD SCHEUER, AND WILLIAM A. CATTERALL* Department of Pharmacology, Box 357280, University of Washington, Seattle, WA 98195-7280 Contributed by William A. Catterall, September 28, 1998 ABSTRACT The voltage-gated sodium channel is the site these sodium channel binding sites are distinct, allosteric of action of more than six classes of neurotoxins and drugs interactions among the sites modulate drug and toxin binding that alter its function by interaction with distinct, allosteri- (10–15). Neurotoxin receptor site 2 binds neurotoxins that cally coupled receptor sites. Batrachotoxin (BTX) is a steroi- cause persistent activation of sodium channels, including ba- dal alkaloid that binds to neurotoxin receptor site 2 and trachotoxin (BTX), veratridine, aconitine, and grayanotoxin causes persistent activation. BTX binding is inhibited allos- (10, 12, 16). BTX is a steroidal alkaloid from the skin secre- terically by local anesthetics. We have investigated the inter- tions of South American frogs of the genus Phyllobates (16). action of BTX with amino acid residues I1760, F1764, and Binding of BTX shifts the voltage dependence of sodium Y1771, which form part of local anesthetic receptor site in channel activation in the negative direction, blocks inactiva- transmembrane segment IVS6 of type IIA sodium channels. tion, and alters ion selectivity (17–20). Its binding to site 2 is Alanine substitution for F1764 (mutant F1764A) reduces a nearly irreversible and is highly dependent on the state of the tritiated BTX-A-20- -benzoate binding affinity, causing a channel with a strong preference for open sodium channels.
    [Show full text]
  • Signed Dissertation Title Page Debi Hudgens
    Di- and Mono- Phenyl Amine Based Sodium Channel Blockers for the Treatment of Pain Debjani Patangia Hudgens Little Rock, AR B.S., University of Arkansas, 2000 A Dissertation presented to the Graduate Faculty of the University of Virginia in Candidacy for the Degree of Doctor of Philosophy Department of Chemistry University of Virginia January, 2007 Acknowledgements I would like to thank the collaborative efforts of several groups who have made this body of work possible. Chapters 2 & 3 All of the [3H]-BTX and [3H]-norepinephrine binding assays were conducted by Novascreen Biosciences, Inc. A great deal of thanks goes the laboratory of Dr. Manoj K. Patel, particularly Catherine Taylor and Dr. Timothy Batts, for the electrophysiological work conducted on sodium channels. Merck, Division of Ion Channel Research, carried out all of the fluorescence based assay work in collaborative efforts with the Brown lab. The NIH screening program at NINDS was responsible for anticonvulsant and toxicity screening in animal models. I would also like to thank the work of Dr. Steve White’s lab, particularly Misty Smith-Yockman, whose efforts in conjunction with NIH has provided for screening in animal models of inflammatory pain. Chapter 5 I would like to thank my advisor, Dr. Milton Brown, for help with the CoMFA model and prediction of future analogues. All of the [3H]-BTX binding assays were conducted by Novascreen Biosciences, Inc. Electrophysiological screening in calcium channels was conducted in the laboratory of Dr. Yong Kim, with special thanks to Nathan Lewis and Maiko Sakai. Chapter 6 I would also like to thank Dr.
    [Show full text]
  • The Pharmacology of Voltage-Gated Sodium Channel Activators
    Accepted Manuscript The pharmacology of voltage-gated sodium channel activators Jennifer R. Deuis, Alexander Mueller, Mathilde R. Israel, Irina Vetter PII: S0028-3908(17)30155-7 DOI: 10.1016/j.neuropharm.2017.04.014 Reference: NP 6670 To appear in: Neuropharmacology Received Date: 13 February 2017 Revised Date: 28 March 2017 Accepted Date: 10 April 2017 Please cite this article as: Deuis, J.R., Mueller, A., Israel, M.R., Vetter, I., The pharmacology of voltage- gated sodium channel activators, Neuropharmacology (2017), doi: 10.1016/j.neuropharm.2017.04.014. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT The Pharmacology of Voltage-gated Sodium channel Activators Jennifer R. Deuis 1,* , Alexander Mueller 1,* , Mathilde R. Israel 1, Irina Vetter 1,2,# 1 Centre for Pain Research, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Qld 4072, Australia 2 School of Pharmacy, The University of Queensland, Woolloongabba, Qld 4102, Australia * Contributed equally # Corresponding author: [email protected] MANUSCRIPT ACCEPTED ACCEPTED MANUSCRIPT Abstract Toxins and venom components that target voltage-gated sodium (Na V) channels have evolved numerous times due to the importance of this class of ion channels in the normal physiological function of peripheral and central neurons as well as cardiac and skeletal muscle.
    [Show full text]
  • ACMT 2020 Annual Scientific Meeting Abstracts – New York, NY
    Journal of Medical Toxicology https://doi.org/10.1007/s13181-020-00759-7 ANNUAL MEETING ABSTRACTS ACMT 2020 Annual Scientific Meeting Abstracts – New York, NY Abstract: These are the abstracts of the 2020 American College of Background: Oral cyanide is a potentially deadly poison and has the Medical Toxicology (ACMT) Annual Scientific Meeting. Included here potential for use by terrorists. There is potential for a mass casualty ex- are 174 abstracts that will be presented in March 2020, including research posure scenario, and currently, there are no FDA-approved antidotes spe- studies from around the globe and the ToxIC collaboration, clinically cifically for oral cyanide poisoning. significant case reports describing new toxicologic phenomena, and en- Hypothesis: We hypothesize that animals treated with oral sodium thio- core research presentations from other scientific meetings. sulfate will have a higher rate of survival vs. control in a large animal model of acute, severe, oral cyanide toxicity. Keywords Abstracts, Annual Scientific Meeting, Toxicology Methods: This is a prospective study that took place at the University of Investigators Consortium, Medical Toxicology Foundation Colorado Anschutz Medical Campus. Nine swine (45–55 kg) were in- strumented, sedated, and stabilized. Potassium cyanide (8 mg/kg KCN) in Correspondence: American College of Medical Toxicology (ACMT), saline was delivered as a one-time bolus via an orogastric tube. Three 10645 N. Tatum Blvd, Phoenix, AZ, USA; [email protected] minutes after cyanide, animals who were randomized to the treatment group received sodium thiosulfate (508.2 mg/kg, 3.25 M solution) via Introduction: The American College of Medical Toxicology (ACMT) re- orogastric tube.
    [Show full text]
  • Free PDF Download
    Eur opean Rev iew for Med ical and Pharmacol ogical Sci ences 2013; 17: 2728-2731 Mad honey intoxication: what is wrong with the blood glucose? a study on 46 patients H. UZUN, H. NARCI 1, I. TAYFUR 2, K.U. KARABULUT 1, O. KARCIOGLU 3 Department of Emergency Medicine, Numune Training and Research Hospital, Trabzon, Turkey 1Department of Emergency Medicine, Baskent University, Medical School, Konya, Turkey 2Department of Emergency Medicine, Haydarpasa Numune Training and Research Hospital, Istanbul, Turkey 3Department of Emergency Medicine Acibadem University, Medical School, Bakirkoy, Istanbul, Turkey Abstract. – OBJECTIVE : This study was de - grow in the eastern Black Sea region of Turkey 1. signed to analyze the characteristics of adult pa - The symptoms of poisoning from this substance, tients with mad honey intoxication, with special emphasis on its effects on vital signs and blood popularly known as mad or bitter honey, are dose- glucose levels. dependent and appear after a specific length of METHODS: Patients admitted to the Emer - time. The typical poisoning picture involves find - gency Department of urban hospital in the Black ings of digestive system irritation, severe bradycar - Sea region of Turkey over the 16-months study dia and hypotension and central nervous system re - period due to mad honey intoxication were in - action 2. A history of honey consumption and clini - cluded. Patients’ demographic and clinical char - acteristics, including age, sex, systolic and dias - cal findings will suggest grayanotoxin poisoning. tolic blood pressure, rhythm at ECG, heart rate, The respiratory effects of grayanotoxin develop blood glucose levels and clinical outcomes were through the central nervous system, and the recorded and analyzed.
    [Show full text]
  • Clinical Review of Grayanotoxin/Mad Honey Poisoning Past and Present
    Clinical Toxicology (2008) 46, 437–442 Copyright © Informa Healthcare USA, Inc. ISSN: 1556-3650 print / 1556-9519 online DOI: 10.1080/15563650701666306 REVIEWLCLT Clinical review of grayanotoxin/mad honey poisoning past and present ABDULKADIRMad Honey Poisoning Past and Present GUNDUZ1, SULEYMAN TUREDI1, ROBERT M. RUSSELL1, and FAIK AHMET AYAZ2 1Karadeniz Technical University Faculty of Medicine, Emergency Medicine, Trabzon, Turkey 2Karadeniz Technical University, Department of Biology, Trabzon, Turkey Grayanotoxin is a naturally occurring sodium channel toxin which enters the human food supply by honey made from the pollen and nectar of the plant family Ericaceae in which rhododendron is a genus. Grayanotoxin/mad honey poisoning is a little known, but well studied, cholinergic toxidrome resulting in incapacitating and, sometimes, life-threatening bradycardia, hypotension, and altered mental status. Complete heart blocks occur in a significant fraction of patients. Asystole has been reported. Treatment with saline infusion and atropine alone is almost always successful. A pooled analysis of the dysrhythmias occurring in 69 patients from 11 different studies and reports is presented. The pathophysiology, signs, symptoms, clinical course, and treatment of grayanotoxin/mad honey poisoning are discussed. In the nineteenth century grayanotoxin/mad honey poisoning was reported in Europe and North America. Currently, documented poisoning from locally produced honey in Europe or North America would be reportable. Possible reasons for this epidemiologic change are discussed. Keywords Grayanotoxin; Rhododendron; Mad honey; Andromedotoxin Introduction Ancient history Mad honey poisoning was first described in 401 BC by Mad honey poisoning is little known outside of Turkey, but it Xenophon, an Athenian author and military commander (10).
    [Show full text]
  • 1 Voltage-Gated Ion Channels and Gating Modifier Toxins William A
    Voltage-gated Ion Channels and Gating Modifier Toxins William A. Catterall,* Sandrine Cestèle,‡ Vladimir Yarov-Yarovoy, Frank H. Yu, Keiichi Konoki, and Todd Scheuer Department of Pharmacology, University of Washington, Seattle, WA 98195-7280 U. S. A. * Corresponding author: Fax: (206) 543-3882; e-mail: [email protected] ‡ Current address: Unité Inserm 607, Canaux Calciques, Fonctions et Pathologies DRDC, Bat. C3, 17 rue des Martyrs. 38054 Grenoble Cedex 09 France 1 Abstract Voltage-gated sodium, calcium, and potassium channels generate electrical signals required for action potential generation and conduction and are the molecular targets for a broad range of potent neurotoxins. These channels are built on a common structural motif containing six transmembrane segments and a pore loop. Their pores are formed by the S5/S6 segments and the pore loop between them and are gated by bending of the S6 segments at a hinge glycine or proline residue. The voltage sensor domain consists of the S1 to S4 segments, with positively charged residues in the S4 segment serving as gating charges. The diversity of toxin action on these channels is illustrated by sodium channels, which are the molecular targets for toxins that act at five or more distinct receptor sites on the channel protein. Both hydrophilic low molecular weight toxins and larger polypeptide toxins physically block the pore and prevent sodium conductance. Hydrophobic alkaloid toxins and related lipid-soluble toxins act at intramembrane sites and alter voltage-dependent gating of sodium channels via an allosteric mechanism. In contrast, polypeptide toxins alter channel gating by voltage-sensor trapping through binding to extracellular receptor sites, and this toxin interaction has now been modeled at the atomic level for a β-scorpion toxin.
    [Show full text]
  • Toxicology Reference Laboratory
    TOXICOLOGY REFERENCE LABORATORY Laboratory User Guide ROOM 708, BLOCK P PRINCESS MARGARET HOSPITAL 2-10 Princess Margaret Hospital Road Lai Chi Kok Tel: 2990 1941 Fax: 2990 1942 http://trl.home Version 6.1 Effective date: 1/July/2014 Contents Contents ..................................................................................................................................................... 2 Introduction ............................................................................................................................................... 4 Staff ............................................................................................................................................................ 5 Honorary Medical Staff .......................................................................................................................... 5 Scientific Staff ........................................................................................................................................ 5 Technical Staff ........................................................................................................................................ 5 Supportive Staff ...................................................................................................................................... 6 How to Make Laboratory Request .......................................................................................................... 7 Instruction for Referring Clinician ........................................................................................................
    [Show full text]
  • Is Grayanotoxin Directly Responsible for Mad Honey Poisoning-Associated Seizures
    Turk J Med Sci 2012; 42 (6): 1086-1092 © TÜBİTAK E-mail: [email protected] Original Article doi:10.3906/sag-1201-14 Is grayanotoxin directly responsible for mad honey poisoning-associated seizures Abdülkadir GÜNDÜZ1, Murat AYDIN1, Metehan AKÇA2,4, Süha TÜRKMEN1, Süleyman TÜREDİ1, Umut ERYİĞİT1, Ali CANSU3,4, Mehmet YILDIRIM2,4 Aim: Th e aim of this study was to investigate the eff ects of grayanotoxin on epileptiform activity in rats. Materials and methods: Forty-two male Sprague Dawley rats were equally divided into 1 of 7 groups. Th irty minutes aft er induction of epileptiform activity induced by penicillin injection, 0.5, 1, 2, 4, or 8 μg of grayanotoxin-III was intracerebroventricularly administered. Epileptiform activity spike frequency and amplitude were converted into numerical data using soft ware following the experiment. Results: Our results show that grayanotoxin reduces epileptiform spike frequency and amplitude in a dose-dependent manner. Five minutes postinjection, grayanotoxin signifi cantly reduced epileptiform activity, especially at higher doses. Th is acute eff ect subsequently declined, but a dose-dependent decrease was observed through the end of the experiment. Th is suggests that the fi rst observed eff ect of grayanotoxin on spikes probably consists of blocking voltage-gated sodium channel inactivation. Conclusion: Grayanotoxin’s suppression of epileptiform activity in this experimental study indicates that grayanotoxin is not directly responsible for mad honey poisoning-associated seizures observed in a clinical context. Key words: Grayanotoxin, mad honey, seizure, experimental epilepsy, ECoG, rat Introduction respiratory system, central nervous system, and Grayanotoxin is found in the leaves and fl owers of endocrine system (4,5).
    [Show full text]