1 Introduction

Total Page:16

File Type:pdf, Size:1020Kb

1 Introduction A Phenotypic and Neuropathological Assessment of the Impact of Fetal and Secondary Adult Re-exposures to Steryl Glucosides in Mice by Opeyemi Christiana Banjo B.Sc., University of California, Davis, 2005 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in The Faculty of Graduate Studies (Neuroscience) THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver) June 2009 © Opeyemi Christiana Banjo, 2009 Abstract Cycad consumption remains one of the strongest etiological factors in the epidemiology of amyotrophic lateral sclerosis-parkinsonism dementia complex (ALS-PDC). Two water insoluble steryl glucosides (stigmasterol β-D-glucoside (SG), and β-sitosterol β-D- glucoside (BSSG)) identified in washed cycad have previously been demonstrated to have neurotoxic effects in both in vitro and in vivo studies. The present study aims to address the variations in age of onset and rate of disease progression, by examining the hypothesis that factors contributing to adult onset diseases may first arise during fetal development. We studied the impact of a prenatal and secondary adult re-exposure to a combination of BSSG and SG on disease onset and progression, and also investigated possible sex differences in disease outcomes. Pregnant CD-1 mice were fed a combination of 0.6mg BSSG and 0.4mg SG on embryonic days 10-11, to target the differentiation of the substantia nigra; other pregnant females received the control diet. Pups were weighed within 24hr of birth, and weekly thereafter. Animals were monitored behaviorally using a series of tests starting at 5 weeks for the duration of the study. At 18 weeks, subsets of both litters were exposed to dietary BSSG and SG in the same doses as before for 15 weeks. Afterwards, animals were perfused and CNS tissue was examined for associated neuropathologies. Behavioral and neuropathological assessments revealed significant differences in the response of adult male and female mice to BSSG and SG exposure. While male mice exposed to BSSG and SG during gestation showed significant weight increases and behavioral deficits irrespective of whether or not they received a secondary exposure, female mice showed marked hyperactivity only if they received BSSG and SG as adults. BSSG and SG exposure also induced significantly decreased tyrosine hydroxylase (TH) labeling in the nigro-striatal pathway, increased apoptosis and gliosis, and resulted in widespread lipid accumulation in male mice; these effects were not observed in female mice. This study demonstrates that developmental exposure to cycad neurotoxins triggers an insult that may elicit a dominant phenotype based on the period of exposure, and that the insult is exacerbated by a secondary exposure, depending on animal sex. ii TABLE OF CONTENTS Abstract........................................................................................................................................ii Table of Contents .......................................................................................................................iii List of Figures............................................................................................................................vii Acknowledgements ....................................................................................................................ix Dedication .................................................................................................................................... x 1 Introduction.............................................................................................................................. 1 1.1 Background: Amyotrophic Lateral Sclerosis – Parkinsonism Dementia C C Complex (ALS-PDC)....................................................................................................... 1 1.1.1 History............................................................................................................. 1 1.1.2 Disease Phenotype and Associated Neuropathology...................................... 2 1.1.3 Other Areas of ALS-PDC Occurrence............................................................ 4 1.2 Disease Etiology ......................................................................................................... 5 1.2.1 Genetic and Environmental Factors................................................................. 5 1.2.2 Cycas Micronesica ........................................................................................... 6 1.2.3 Putative Cycad Toxins ...................................................................................... 6 1.2.4 An Animal Model of ALS-PDC ....................................................................... 8 1.2.5 The FeBAD Hypothesis.................................................................................... 9 1.3 Rationale and Hypotheses Tested ............................................................................... 11 1.3.1 Rationale .......................................................................................................... 11 1.3.2 Hypotheses....................................................................................................... 11 2 Materials and Methods.......................................................................................................... 14 2.1 Materials ..................................................................................................................... 14 2.1.1 Chemical Reagents........................................................................................... 14 2.1.2 Laboratory Supplies......................................................................................... 15 2.1.3 Primary and Secondary Antibodies ................................................................. 16 2.1.4 Behavioral Testing Equipment ........................................................................ 16 2.2 Methods....................................................................................................................... 16 2.2.1 Cycad Steryl Glucoside Synthesis ................................................................... 16 2.2.2 Animals............................................................................................................ 17 iii 2.2.3 Steryl Glucoside Feeding................................................................................. 19 2.2.4 Animal Behavior Testing................................................................................. 20 2.2.5 Animal Sacrifice and Tissue Processing.......................................................... 23 2.2.6 Nissl – Lower Motor Neuron Quantification................................................... 24 2.2.7 Fluorescence Antibody Staining...................................................................... 25 2.2.8 Immunoperoxidase Antibody Staining in Lumbar Spinal Cord ...................... 27 2.2.9 Immunoperoxidase Antibody Staining in Brain Sections................................ 30 2.2.10 Tyrosine Hydroxylase Immunohistochemistry.............................................. 31 2.2.11 Lipid Accumulation - Oil Red O ................................................................... 32 2.2.12 Magnetic Resonance Microscopy (MRM)..................................................... 34 2.2.13 Statistical Analyses ........................................................................................ 34 3 Effects of Prenatal Exposure to BSSG and SG on Mouse Behavior 3.1 Aims............................................................................................................................ 36 3.2 Results......................................................................................................................... 36 3.2.1 Fetal Exposure to BSSG and SG Induces Considerable Increases ----- --------------Body Weight ............................................................................................................ 37 3.2.2 The Impact of Fetal Exposure to BSSG and SG on Spinal Reflexes and M Muscle Strength........................................................................................................ 37 3.2.3 Fetal Exposure to BSSG and SG Induces Changes in Mice Gait and Exploratory Patterns.................................................................................................. 37 3.3 Discussion................................................................................................................... 38 3.4 Conclusions................................................................................................................. 40 4 Effects of Postnatal Secondary Re-exposure to Dietary BSSG and SG on Adult Male Mice .................................................................................................................................. 58 4.1 Aims........................................................................................................................... 58 4.2 Results........................................................................................................................ 58 4.2.1 Male Mice Exposed to BSSG and SG During Development Maintain 000 Larger Body Weights................................................................................................ 58 4.2.2 “Prenatal Exposure Only” Male Mice Show Similar Behavioral Trends 000 as Group Exposed Both Pre- and Post-natally.......................................................... 59 iv 4.2.3 Decrease in Tyrosine Hydroxylase Immunoreactivity
Recommended publications
  • Nervous Tissue
    Department of Histology and Embryology Medical faculty KU Bratislava NERVOUS TISSUE RNDr. Mária Csobonyeiová, PhD ([email protected]) Nerve tissue neurons /main cells/ (perikaryon = cell body=soma,dendrites,axon), 4 -150 µm glial cells /supporting cells/ - 10 times more abudant CNS- oligodendrocytes, astrocytes, ependymal cells,microglia PNS - Schwann cells, satelite cells Neuron independentNeuron anatomical and functional unit responsible for: receiving of different types of stimuli transducing them into the nerve impulses conducting them to the nerve centers development – embryonal neuroectoderm Morphology of the neurons Pseudounipolar neuron! (spinal ganglion) Methods used in neurohistology Staining methods: Luxol blue and cresyl violet (nucleus+nucleolus+Nissl body) Luxol blue (myelin sheath) and nuclear red (nucleus + nucleolus+Nissl body) Impregnations according - Holmes – neurons, axon, dendrites - neurofibrils (brown-violet) Golgi – neurons + astrocytes (black) with golden background Cajal – astrocytes (black) with red background Rio del Hortega – microglia (black) with gray-violet background OsO4 - myelin sheath (black), staining for lipids and lipoproteins (myelin) Microglia (phagocytosis) Astrocytes (supporting role, Oligodendrocytes nutrition, healing (formation of myelin of defects - glial sheath) scars, formation of BBB) Ependymal cells (regulation of stable chemical constitution of CSF) CSN Gray matter: White matter: - bodies of neurons, dendrites - myelinated and unmyelinated axons - initial portion
    [Show full text]
  • Vocabulario De Morfoloxía, Anatomía E Citoloxía Veterinaria
    Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) Servizo de Normalización Lingüística Universidade de Santiago de Compostela COLECCIÓN VOCABULARIOS TEMÁTICOS N.º 4 SERVIZO DE NORMALIZACIÓN LINGÜÍSTICA Vocabulario de Morfoloxía, anatomía e citoloxía veterinaria (galego-español-inglés) 2008 UNIVERSIDADE DE SANTIAGO DE COMPOSTELA VOCABULARIO de morfoloxía, anatomía e citoloxía veterinaria : (galego-español- inglés) / coordinador Xusto A. Rodríguez Río, Servizo de Normalización Lingüística ; autores Matilde Lombardero Fernández ... [et al.]. – Santiago de Compostela : Universidade de Santiago de Compostela, Servizo de Publicacións e Intercambio Científico, 2008. – 369 p. ; 21 cm. – (Vocabularios temáticos ; 4). - D.L. C 2458-2008. – ISBN 978-84-9887-018-3 1.Medicina �������������������������������������������������������������������������veterinaria-Diccionarios�������������������������������������������������. 2.Galego (Lingua)-Glosarios, vocabularios, etc. políglotas. I.Lombardero Fernández, Matilde. II.Rodríguez Rio, Xusto A. coord. III. Universidade de Santiago de Compostela. Servizo de Normalización Lingüística, coord. IV.Universidade de Santiago de Compostela. Servizo de Publicacións e Intercambio Científico, ed. V.Serie. 591.4(038)=699=60=20 Coordinador Xusto A. Rodríguez Río (Área de Terminoloxía. Servizo de Normalización Lingüística. Universidade de Santiago de Compostela) Autoras/res Matilde Lombardero Fernández (doutora en Veterinaria e profesora do Departamento de Anatomía e Produción Animal.
    [Show full text]
  • The “Road Map”
    PRACTICAL ROADMAP NERVOUS TISSUE DR N GRAVETT NEURONS • MOTOR • SENSORY Anterior (ventral) horn Dorsal root of spinal of spinal cord cord Multipolar Pseudounipolar ANTERIOR HORN CELLS • Slide 64 Spinal Cord (vervet monkey) Stain: Kluver and Berrera Technique NOTE: with this technique, myelin stains dark blue and basophilic substances such as rER and nuclei stain violet. In this case we use “blue” and “purple” to describe the staining and not eosinophilic and basophilic. SPINAL CORD Anterior Ventral Horn Arachnoid Ventricle Pia Mater Grey Matter White Matter Posterior Horn Dura Mater Dorsal ANTERIOR HORN CELL Neuropil Cell Body Dendrite Vesicular Nucleus Nucleolus Nucleus of Nissl Bodies Neuroglial Cell ANTERIOR HORN CELL Neuropil Cell Body Vesicular Nucleus Nucleolus Nissl Body Nucleus of Neuroglial Cell Dendrite Nissl Body Axon Hillock Axon SPINAL (DORSAL ROOT) GANGLION CELLS • Slide 62 Spinal Ganglion Stain: H&E NOTE: The spinal ganglion is also known as the dorsal root ganglia and contains pseudounipolar neuron cell bodies. SPINAL (DORSAL ROOT) GANGLIA Cell Bodies Processes (Axons and Dendrites) SPINAL (DORSAL ROOT) GANGLIA Cell Bodies Processes (Axons and Dendrites) NOTE: The neuronal cell bodies of the dorsal root ganglia are “clumped” together, and one cannot see any processes entering or leaving the cell bodies. The processes (axons and dendrites) are seen towards the edge/periphery of the group of cell bodies. SPINAL (DORSAL ROOT) GANGLIA Satellite cells (arranged in ring like fashion around the cell body) Cell Body Nucleolus Vesicular Fine Granular Nucleus Nissl Substance Nucleus of Satellite cell PERIPHERAL BRANCH OF A SPINAL NERVE • Slide 32 Median Nerve Stain: Mallory’s Technique NOTE: Three dyes are used in Mallory’s technique, which results in collagen fibres (such as connective tissue) staining blue, the “neurokeratin” staining red, and nuclei staining reddish-orange PERIPHERAL NERVE Myelinated Axons Vein L.S.
    [Show full text]
  • Review Chromatolysis: Do Injured Axons
    Preprints (www.preprints.org) | NOT PEER-REVIEWED | Posted: 16 February 2018 doi:10.20944/preprints201802.0111.v1 Review Chromatolysis: Do Injured Axons Regenerate Poorly when Ribonucleases Fragment or Degranulate Rough Endoplasmic Reticulum, Disaggregate Polyribosomes, Degrade Monoribosomes and Lyse RNA? Running title: Which ribonucleases limit axon regeneration? Lawrence David Falcon Moon a a Neurorestoration Group, Wolfson Centre for Age-Related Diseases, 16-20 Newcomen Street, London, SE1 1UL, United Kingdom [email protected] Acknowledgments: This work was supported by a grant from the Wings for Life foundation and through a grant to the “AxonRepair” consortium from ERA-NET NEURON that is co-sponsored by the Medical Research Council. Thanks to Emeritus Professor Thomas Sears and Professor Simone Di Giovanni for providing feedback on a draft. Abstract: After axonal injury, chromatolysis (fragmentation of Nissl substance) occurs in both intrinsic neurons (whose processes are within the CNS) and extrinsic neurons (whose axons extend outside the CNS). Electron microscopy shows that chromatolysis involves fission of the rough endoplasmic reticulum. In intrinsic neurons (which do not regenerate axons) or in extrinsic neurons denied axon regeneration, chromatolysis is often accompanied by degranulation (loss of ribosomes from rough endoplasmic reticulum), disaggregation of polyribosomes and degradation of monoribosomes into dust-like particles. Ribosomes and rough endoplasmic reticulum may also be degraded in autophagic vacuoles by Ribophagy and Reticulophagy, respectively. In other words, chromatolysis is disruption of parts of the protein synthesis infrastructure. Whereas some neurons may show transient or no chromatolysis, severely injured neurons can remain chromatolytic and never again synthesise normal levels of protein; some may atrophy or die.
    [Show full text]
  • A Translation Insight Into the Scientific Textbook
    NEUROPHYSIOLOGY: A TRANSLATION INSIGHT INTO THE SCIENTIFIC TEXTBOOK MASTER’S DISSERTATION ON MEDICAL TRANSLATION PRACTICE MÁSTER UNIVERSITARIO EN TRADUCCIÓN MÉDICO-SANITARIA (2017/2018) Esther Andrés Caballo Supervisors: Dr. Laura Carasusán Senosiáin (Universitat Jaume I) Dr. Rocío Baños-Piñero (CenTraS-UCL) Acknowledgments This dissertation would have not been possible but for the support of many people. In the first place, I am particularly grateful to the Master’s faculty at UJI who gave me the insight and educational input into the medical translation that is needed for competence and subject-knowledge acquisition to enter into this profession. I would like to thank them all personally since I have most learnt from their lectures, feedback on my translation work, and recommendations during the master’s course of studies. Secondly, I am extremely grateful to the Erasmus+ Master Exchange Programme, whereby a Higher Education Learning Agreement for Studies was signed by and between Universitat Jaume I (Spain) and University College London (UK), which gave me the great opportunity of a five-month stay at University College London. In this prestigious university, particularly in the Centre for Translation Studies (CenTraS), I have done my translation practice on-line, conducted my research and written down this dissertation, while making full employ of the numberless resources available at the Main and Science Libraries and the Institute of Physiology at UCL. I highly appreciate the welcoming and availability of CenTraS’ administrators and teaching staff, and specially, the priceless support of my dissertation supervisor. Thirdly, I must acknowledge the wisdom of the masters, and devotedly thank Dr. Ignacio Navascués and their team, Dr.
    [Show full text]
  • Comparative Light Microscopic Study of Trigeminal Ganglion Neurons in Mammals
    Current Neurobiology 2010, 1 (1): 25-29 Comparative Light Microscopic Study of Trigeminal Ganglion Neurons in Mammals M. Naushad A Dilkash, Syed Sayeed Ahmed* and Aijaz Ahmed Khan Dept. of Anatomy, JN Medical College, Aligarh Muslim University, Aligarh, India *Dept. of Oral and Maxillofacial Surgery, Dr. Z A Dental College, AMU, Aligarh, India. Abstract Trigeminal ganglion (TRG) consists of collection of primary sensory neurons. The different subsets of neurons have been identified on the basis of morphological and neurochemical characteristics. It remains to be resolved as to whether the various neuronal subsets remain alike across the mammalian species and if there exists some species specific characteristic neurons. The present study was conducted on adult mammals (rat, rabbit, and goat) of either sex. TRG of both sides were procured and fixed in 10% buffered formalin and processed for paraffin embedding. 10 µm thick sections stained with Haematoxylin and Eosin were examined under light microscope and relevant findings were recorded in photomicrographs. It was noticed that the main cellular constituents (neuron and glia) of TRG could be easily identified and features of most of the neurons matched with earlier light microscopic descriptions [1, 2]. However, few neurons in the present study revealed certain additional features. For example – in the medium size neuron, large Nissl granules formed single peripheral ring; in the medium and large sized neurons, coarse Nissl granules formed two concentric (perinuclear and peripheral) rings; and a couple of neurons appeared to share common sheath – a kin to binucleate neurons. In addition, the neuronal somatic size appeared to have direct relationship with the body size of the animal.
    [Show full text]
  • NIH Public Access Author Manuscript Brain Res
    NIH Public Access Author Manuscript Brain Res. Author manuscript; available in PMC 2010 April 17. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Brain Res. 2009 April 17; 1266: 29±36. doi:10.1016/j.brainres.2009.02.031. Morphological and ultrastructural features of Iba1-immunolabeled microglial cells in the hippocampal dentate gyrus Lee A. Shapiro1,2, Zachary D. Perez3, Maira L. Foresti2, Gabriel M. Arisi2, and Charles E. Ribak3 1 Department of Surgery, Division of Neurosurgery, Texas A&M University College of Medicine 2 Scott & White Hospital, Neuroscience Research Institute, Temple, TX 3 Department of Anatomy and Neurobiology, University of California at Irvine, Irvine, CA Abstract Microglia are found throughout the central nervous system, respond rapidly to pathology and are involved in several components of the neuroinflammatory response. Iba1 is a marker for microglial cells and previous immunocytochemical studies have utilized this and other microglial-specific antibodies to demonstrate the morphological features of microglial cells at the light microscopic level. However, there is a paucity of studies that have used microglial-specific antibodies to describe the ultrastructural features of microglial cells and their processes. The goal of the present study is to use Iba1 immuno-electron microscopy to elucidate the fine structural features of microglial cells and their processes in the hilar region of the dentate gyrus of adult Sprague-Dawley rats. Iba1-labeled cell bodies were observed adjacent to neurons and capillaries, as well as dispersed in the neuropil. The nuclei of these cells had dense heterochromatin next to the nuclear envelope and lighter chromatin in their center.
    [Show full text]
  • Índice De Denominacións Españolas
    VOCABULARIO Índice de denominacións españolas 255 VOCABULARIO 256 VOCABULARIO agente tensioactivo pulmonar, 2441 A agranulocito, 32 abaxial, 3 agujero aórtico, 1317 abertura pupilar, 6 agujero de la vena cava, 1178 abierto de atrás, 4 agujero dental inferior, 1179 abierto de delante, 5 agujero magno, 1182 ablación, 1717 agujero mandibular, 1179 abomaso, 7 agujero mentoniano, 1180 acetábulo, 10 agujero obturado, 1181 ácido biliar, 11 agujero occipital, 1182 ácido desoxirribonucleico, 12 agujero oval, 1183 ácido desoxirribonucleico agujero sacro, 1184 nucleosómico, 28 agujero vertebral, 1185 ácido nucleico, 13 aire, 1560 ácido ribonucleico, 14 ala, 1 ácido ribonucleico mensajero, 167 ala de la nariz, 2 ácido ribonucleico ribosómico, 168 alantoamnios, 33 acino hepático, 15 alantoides, 34 acorne, 16 albardado, 35 acostarse, 850 albugínea, 2574 acromático, 17 aldosterona, 36 acromatina, 18 almohadilla, 38 acromion, 19 almohadilla carpiana, 39 acrosoma, 20 almohadilla córnea, 40 ACTH, 1335 almohadilla dental, 41 actina, 21 almohadilla dentaria, 41 actina F, 22 almohadilla digital, 42 actina G, 23 almohadilla metacarpiana, 43 actitud, 24 almohadilla metatarsiana, 44 acueducto cerebral, 25 almohadilla tarsiana, 45 acueducto de Silvio, 25 alocórtex, 46 acueducto mesencefálico, 25 alto de cola, 2260 adamantoblasto, 59 altura a la punta de la espalda, 56 adenohipófisis, 26 altura anterior de la espalda, 56 ADH, 1336 altura del esternón, 47 adipocito, 27 altura del pecho, 48 ADN, 12 altura del tórax, 48 ADN nucleosómico, 28 alunarado, 49 ADNn, 28
    [Show full text]
  • The Fine Structure of the Lateral Vestibular Nucleus in the Rat
    THE FINE STRUCTURE OF THE LATERAL VESTIBULAR NUCLEUS IN THE RAT I. Neurons and Neuroglial Cells CONSTANTINO SOTELO and SANFORD L. PALAY Downloaded from http://rupress.org/jcb/article-pdf/36/1/151/1068343/151.pdf by guest on 02 October 2021 From the Department of Anatomy, Harvard Medical School, Boston, Massachusetts 02115. Dr. Sotelo's present address is Laboratoire de Biologie Animale, Facult6 des Sciences de Paris, Paris, France ABSTRACT The lateral vestibular nucleus consists of multipolar isodendritic neurons of various sizes The distal segments of some dendrites display broad expansions packed with slender mito- chondria and glycogen particles. These distinctive formations are interpreted as being growing tips of dendrites, and the suggestion is advanced that they are manifestations of architectonic plasticity in the mature central nervous system. Unlike large neurons else- where, the giant cells (Deiters) contain small Nissl bodies interconnected in a dense mesh- work. The Nissl substance is characterized by randomly arranged cisterns of the endoplasmic reticulum and by a high proportion of free ribosomes. Whether attached or free, ribosomes usually cluster in groups of four to six, and larger polysomal arrays are rare. Free ribosomal clusters also occur in the axon hillock and the initial segment. The neuronal perikarya contain distinctive inclusions consisting of a ball of neurofilaments enveloped by a complex honeycombed membrane. The failure of these fibrillary inclusions to stain with silver sug- gests that the putative argyrophilia of neurofilaments may reside in an inconstant matrix surrounding them. Giant cells of Deiters are in intimate contact with two kinds of cellular elements-astroglial processes and synaptic terminals.
    [Show full text]
  • An Ultrastructural Comparison of Axotomised Dorsal Root Ganglion Neurons with Allowed Or Denied Reinnervation of Peripheral Targets Neuroscience, 2013; 228:163-178
    SUBMITTED VERSION Johnson, Ian Paul; Sears, T. A. Target-dependence of sensory neurons: An ultrastructural comparison of axotomised dorsal root ganglion neurons with allowed or denied reinnervation of peripheral targets Neuroscience, 2013; 228:163-178 © 2012 IBRO. Published by Elsevier Ltd. All rights reserved. NOTICE: this is the author’s version of a work that was accepted for publication in Neuroscience. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Neuroscience, 2013; 228:163-178. DOI: 10.1016/j.neuroscience.2012.10.015 PERMISSIONS http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy#pre-print Elsevier's Policy: An author may use the preprint for personal use, internal institutional use and for permitted scholarly posting. In general, Elsevier is permissive with respect to authors and electronic preprints. If an electronic preprint of an article is placed on a public server prior to its submission to an Elsevier journal or where a paper was originally authored as a thesis or dissertation, this is not generally viewed by Elsevier as “prior publication” and therefore Elsevier will not require authors to remove electronic preprints of an article from public servers should the article be accepted for publication in an Elsevier journal. However, please note that Cell Press and The Lancet have different preprint policies and will not consider articles that have already been posted publicly for publication.
    [Show full text]
  • Chromatolysis: Do Injured Axons Regenerate Poorly When Ribonucleases Attack Rough Endoplasmic Reticulum, Ribosomes and RNA? Developmental Neurobiology
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by King's Research Portal King’s Research Portal DOI: 10.1002/dneu.22625 Document Version Publisher's PDF, also known as Version of record Link to publication record in King's Research Portal Citation for published version (APA): Moon, L. D. F. (2018). Chromatolysis: Do injured axons regenerate poorly when ribonucleases attack rough endoplasmic reticulum, ribosomes and RNA? Developmental Neurobiology. https://doi.org/10.1002/dneu.22625 Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version for pagination, volume/issue, and date of publication details. And where the final published version is provided on the Research Portal, if citing you are again advised to check the publisher's website for any subsequent corrections. General rights Copyright and moral rights for the publications made accessible in the Research Portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognize and abide by the legal requirements associated with these rights. •Users may download and print one copy of any publication from the Research Portal for the purpose of private study or research. •You may not further distribute the material or use it for any profit-making activity or commercial gain •You may freely distribute the URL identifying the publication in the Research Portal Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim.
    [Show full text]
  • From the Poliomyelitis Research Center, Department of Epidemiology, Johns Hopkins University, Baltimore) PLATES 23 ~O 27
    CORE Metadata, citation and similar papers at core.ac.uk Provided by PubMed Central THE REGENERATIVE CYCLE OF MOTONEURONS, WITH SPECIAL REFERENCE TO PHOSPHATASE ACTIVITY* BY DAVID BODIAN, M.D., A~D ROBERT C. MELLORS, M.D. (From the Poliomyelitis Research Center, Department of Epidemiology, Johns Hopkins University, Baltimore) PLATES 23 ~o 27 (Received for publication, January 30, 1945) I. Ttt~ REGENERATIVE CYCLE OF MOTON~IYRONS I The phenomenon of axon regeneration presents an exceptional opportunity for study of the mechanisms of cytoplasmic growth and reorganization in highly differen- tiated cells. In motor nerve cells, for example, a large part of the cytoplasm, the enormously long axon, can be conveniently amputated by peripheral nerve transection. The subsequent structural transformations in perikaryon and axon, and the chemical changes which parallel them, have been the subject of numerous histochemical as well as histological investigations. However, such studies of the consequences of nerve transection have generally treated separately the events of degeneration and regen- eration of the axon, and the retrograde reaction of the cell body, commonly called chromatolysis or chromolysis because of the prominent decrease of basophilic material in the cytoplasm of the cell body. The complexities of the reaction of the nerve cell to axon amputation are well known. A large variability of response is found among the many nerve cell types present in various parts of the nervous system, as well as in homologous cell types in different animal species, or under varying conditions of age and physiological state (1-3). For example, the chromatolytic reaction in the cell body which occurs in most vertebrate cells, and apparently in some invertebrate neurons (4), after axon amputa- tion, has been said not to occur in anterior horn cells of the rabbit (2, 5, 6), although we have found it to be present largely in mild degree in such cells in adult rabbits.
    [Show full text]