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228 Pages·1998·17.077 MB·English
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MOLECULAR AND CELLULAR MECHANISMS OF NEURONAL PLASTICITY Basic and Clinical Implications ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Editorial Board: NATHAN BACK, State University of New York at Buffalo IRUN R. COHEN, The Weizmann Institute of Science DAVID KRITCHEVSKY, Wistar Institute ABEL LAJTHA, N. S. Kline institute lor Psychiatric Research RODOLFO PAOLETTI, Universily ofMilQIl Recent Volumes in this Series Volume 443 ADV ANCES IN LACTOFERRIN RESEARCH Edited by Genevieve Spik, Dominique Legrand, Joel Mazurier, Annick Pierce, and Jean-Paul Perraudin Volume 444 REPRODUCTIVE TOXICOLOGY: In Vitro Germ Cell Developmental Toxicology, from Science to Social and Industrial Demand Edited by Jesus del Mazo Volume 445 MATHEMATICAL MODELING IN EXPERIMENT AL NUTRITION Edited by Andrew J. Clifford and Hans-Georg Muller Volume 446 MOLECULAR AND CELLULAR MECHANISMS OF NEURONAL PLASTICITY: Basic and Clinical Implications Edited by Yigal H. Ehrlich Volume 447 LIPOXYGENASES AND THEIR METABOLITES: Biological Functions Edited by Santosh Nigam and Cecil R. Pace-Asciak Volume 448 COPPER TRANSPORT AND ITS DISORDERS: Molecular and Cellular Aspects Edited by Arturo Leone and Julian F. B. Mercer Volume 449 VASOPRESSIN AND OXYTOCIN: Molecular, Cellular, and Clinical Advances Edited by Hans H. Zingg, Charles W. Bourque, and Daniel G. Bichet Volume 450 ADV ANCES IN MODELING AND CONTROL OF VENTILA nON Edited by Richard 1. Hughson, David A. Cunningham, and James Duffin Volume 451 GENE THERAPY OF CANCER Edited by Peter Walden, Uwe Trefzer, Wolfram Sterry, and Farzin Farzaneh Volume 452 MECHANISMS OF LYMPHOCYTE ACTIVATION AND IMMUNE REGULATION VII: Molecular Determinants of Microbial Immunity Edited by Sudhir Gupta, Alan Sher, and Rafi Ahmed A Continuation Order Plan is available for this series. A continuation order will bring delivery of each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further information please contact the publisher. MOLECULAR AND CELLULAR MECHANISMS OF NEURONAL PLASTICITY Basic and Clinical Implications Edited by Yigal H. Ehrlich The College of Staten Island ofThe City University of New York, and The CSIIIBR Center for Developmental Neuroscience Staten Island, New York, and The City University Graduate School New York, New York SPRINGER SCIENCE+BUSINESS MEDIA, LLC Llbrary of Congress Cataloglng-In-Publlcatlon Data Molecular and cellular mechanlsas of neuronal plasticity , basic and cllnical lmpllcatlons 1 edlted by Vlgal H. Ehrllch. p. c •. -- (Advances in experimental aedicine and biology : v. 446) "Proceedings of the Neurosclence SymposiuM on Molecular and Cellular Mechanisms of Neuronal Plasticlty. held Oecember 4. 1996. in Staten Is~and, New Vork"--T.p. verso. Includes bibliographical references and index. ISBN 978-1-4613-7209-7 ISBN 978-1-4615-4869-0 (eBook) DOI 10.1007/978-1-4615-4869-0 1. Neuroplastlcity--Congresses. 2. Molecular neurobiology -Congresses. 3. Neurons--Congresses. 1. Ehrllch, Vlgal H. II. Neurosclence Syaposlum an Molecular and Cellular Mechanlsms of Neuronal Plastlclty (1996 , Staten Island. New York. N.V.l III. Ser Ies. [ONLM, 1. Neuronal Plasticlty--physlology congresses. 2. Neurons -physlology congresses. Hl A0559 v.446 19961 QP363.3.M65 1996 61 l' .0166--dc21 ONLM/OLC for Llbrary of Congress 96-31763 CIP Proceedings of the Neuroscience Symposium on Molecular and Cel\ular Mechanisms of Neuronal Plasticity, held Oecember 4, 1996, in Staten Island, New York, with chapters written by symposium speakers and additional invited authors during 1997 and updated through March 1998. ISBN 978-1-4613-7209-7 © 1998 Springer Science+Business Media New York Originally published by Kluwer Academic / Plenum Publishers in 1998 Softcover reprint of the hardcover 1s t edition 1998 AII rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher PREFACE Cells in the nervous system have the capability of undergoing extremely long-lasting alterations in response to hormonal, pharmacological and environmental stimulations. The mechanisms underlying this neuronal plasticity are activated by experiential inputs and operate in the process of learning and the formation of memories in the brain. Numerous studies have proven the biological basis of memory formation and have begun to identify the biochemical traces and cellular circuits that are formed by experience, and which par ticipate in the storage of information in the brain, its retention for long durations, and its retrieval upon demand. Furthermore, the elucidation of molecular and cellular mecha nisms operating in the adaptive processes which underlie neuronal plasticity have begun to yield novel strategies in the diagnosis and treatment of neurological diseases and neuro phychiatric disorders. A major practical outcome of these investigations has been the emergence of a new generation of therapeutic agents; memory enhancing drugs developed on the basis of understanding the biochemistry, cellular biology and molecular genetics of processes underlying neuronal plasticity. These studies are at the focus of the present Vol ume, which has emerged initially from a Symposium held at the College of Staten Island of The City University of New York on December 4, 1996. This Volume includes contribu tions submitted during 1997 and early 1998 by presenting speakers of the Symposium, as well as additional invited authors who conduct unique studies in this area. As in my pre vious editorial work (Ehrlich et aI., Volume 116 and Volume 221 of Advances in Experi mental Medicine and Biology, Plenum Press, New York), I hope that the readers will find here a useful source of information and ideas for stimulating studies which will serve to further narrow the gap between basic neuroscience research and its clinical implications. One of the guidelines in selecting the contributions invited as chapters for this Vol ume has been the presentation of research areas that have not been highlighted in previous books on this topic. Thus, in addition to studies on the involvement of functional proteins (enzymes, receptors) in neuronal adaptation, this Volume presents recent developments on the critical roles of bioactive lipids and nucleotides in these processes. In addition to the widely studied role of second messengers-regulated protein kinases in mechanisms under lying neuronal plasticity, a review of studies on extracellular protein phosphorylation sys tems operating on the surface of brain neurons is presented in this Volume. Together with studies of mammalian brain, the advantages of investigating avian hippocampus as a model to study synaptic plasticity is presented here. While the NMDA sub-type of gluta mate receptors has been a major focus of studies on hippocampal synaptic plasticity, a chapter on the clinical impact of studies on the role of metabotropic glutamate receptors in v Preface the plasticity of excitatory responses in the hippocampus is presented here as a bridge be tween the two sections of the Volume. The first section presents studies of basic mecha nisms operating in a wide-range of adaptive processes. These include synaptic changes responsible for associative memory, long-term habituation, long-term potentiation, neuro nal development and programmed neuronal cell-death (apoptosis). The second section of this Volume, beginning with Chapter 9, presents recent advances in investigations that have demonstrated the clinical implications of this research. These include: state-of-the-art use of transgenic models in studies of molecular and cellular mechanisms implicated in fa milial Alzheimer's disease and Amyotropic Lateral Sclerosis (ALS); studies of specific proteins implicated in Alzheimer's disease-including an adapter that binds to the l3-amy loid precursor protein (I3-APP) and the microtubular protein Tau and its membrane-bound counterpart. The advantages of using cell culture models for elucidating the causes of neuronal degeneration and for identifying mechanisms of neuroprotection are also pre sented among the chapters in the section on Clinical Implications. The Editor wishes to express here his thanks to a few of the many individuals who contributed to the organization of the Symposium: the President of the College of Staten Island (CSI) Dr. Marlene Springer and the Vice-President for Academic Affairs and Pro vost Dr. Mirella Affron, the Director of the New York State Institute of Basic Research in Developmental Disabilities (lBR) Dr. Henryk M. Wisniewski, the Deputy Director of the CSI/IBR Center for Developmental Neuroscience Dr. E. Trenkner, and the Dean of Sci ence at CSI Dr. Martin Zeldin. Special thanks are due to the staff of the Center for Per forming Arts of CSI, and in particular to the secretary of the Program in Neuroscience of CSI, Rosa Shirippa for her tireless efforts. Finally, the support and help of my colleague and friend Dr. Elizabeth Kornecki in the preparation of this Volume is acknowledged with affection and admiration. Yigal H. Ehrlich CONTENTS I. Molecular Specificity of Synaptic Changes Responsible for Associative Memory Daniel L. Alkon 2. Behavioral and Mechanistic Bases of Long-Term Habituation in the Crab Chasmagnathus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 Daniel Tomsic, Arturo Romano, and Hector Maldonado 3. Bioactive Lipids and Gene Expression in Neuronal Plasticity 37 Nicolas G. Bazan 4. Surface Protein Phosphorylation by Ecto-Protein Kinases: Role in Neuronal Development and Synaptic Plasticity ... . . . . . . . . . . . . . . . . . . . . . . . . . . . 51 Yigal H. Ehrlich, Michael V. Hogan, Zofia Pawlowska, Andrzej Wieraszko, Ethel Katz, Tomasz Sobocki, Anna Babinska, and Elizabeth Komecki 5. Extracellular ATP-Induced Apoptosis in PC12 Cells. . . . . . . . . . . . . . . . . . . . . . . 73 Albert Y. Sun and Yong-Mei Chen 6. The Role of the Neural Growth Associated Protein B-50/Gap-43 in Morphogenesis ............................................... 85 L. H. J. Aarts, P. Schotman, J. Verhaagen, L. H. Schrama, and W. H. Gispen 7. Avian Hippocampus as a Model to Study Spatial Orientation-Related Synaptic Plasticity .................................................... 107 Andrzej Wieraszko 8. Metabotropic Glutamate Receptors in the Plasticity of Excitatory Responses in the Hippocampus: Clinical Impact ................................ 13 I Lisa R. Merlin 9. Familial Amyotrophic Lateral Sclerosis and Alzheimers Disease: Transgenic Models...................................................... 145 Philip C. Wong, David R. Borchelt, Michael K. Lee, Carlos A. Pardo, Gopal Thinakaran, Lee J. Martin, Sangram S. Sisodia, and Donald L. Price vii viii Contents 10. Proteins Implicated in Alzheimer Disease: The Role ofFE65, a New Adapter which Binds to ~-Amyloid Precursor Protein ....................... 161 Kira S. Ermekova, Alex Chang, Nicola Zambrano, Paola de Candia,Tommaso Russo, and Marius Sudol 11. Influence of Phospholipids and Sequential Kinase Activities on Tau in Vitro 181 Thomas B. Shea and Fatma 1. Ekinci 12. Cell Culture Models of Neuronal Degeneration and Neuroprotection: Implications for Parkinson's Disease .............................. 203 Efthimia T. Kokotos Leonardi and Catherine Mytilineou 13. Aging and Dementia of the Alzheimer Type: In Persons with Mental Retardation 223 Henryk M. Wisniewski and Wayne Silverman Index 227 1 MOLECULAR SPECIFICITY OF SYNAPTIC CHANGES RESPONSIBLE FOR ASSOCIATIVE MEMORY Daniel L. Alkon Laboratory of Adaptive Systems NINDS, NIH Bethesda, Maryland INTRODUCTION Specificity of molecular mechanisms for synaptic weight regulation is critical for understanding the cellular basis of learning and memory. Thus, while we have known for decades that protein synthesis is involved in long-term memory (Flexner et aI., 1963; Hy den et aI., 1965; Agranoff et aI., 1966; Matthies, 1989; Van der Zee et aI., 1992; Nelson and Alkon, 1992; see Kandel, this volume), protein synthesis is also necessary for so many cellular functions that its direct contribution to memory function remains obscure. Here, however, we describe a new signalling protein, Calexcitin, which powerfully and specifi cally regulates synaptic weight as well as synaptic sign and is activated by a molecular cascade more directly implicated in associative learning of diverse molluscan and mam malian species. This cascade begins when temporally related training stimuli (e.g. an auditory tone and a touch stimulus to the cornea) elicit temporally related synaptic signals that in turn elicit temporally related second messengers such as Ca++, DAG (diacyl glycerol), and AA (arachidonic acid). Temporally associated second messengers activate protein kinase C (PKC) through its translocation to the inner surface of neuronal mem branes (and possibly membranes of subcellular organelles such as the ER). Membrane-as sociated PKC, now sensitive to low levels of Ca -+ (0.1-1.0 uM), phosphorylates critical signaling proteins such as the recently sequenced cp20 (now called "Calexcitin"), the first known protein to bind both Ca++ and GTP. Calexcitin, shown to be a high affinity substrate of Ca++-dependent isozymes of PKC (particularly the a-isozyme), when phosphorylated during learning, also becomes membrane associated and inactivates voltage-dependent K+ channels (such as lA' Ie. etc.). Recent experiments (Weh et aI., in press) also implicate Cal excitin in the regulation of Ca++ release from the endoplasmic reticulum and thus further CaH-mediated transformations of synaptic weight and perhaps structure. Still other recent experiments (Cavallero et aI., Soc.for Neuroscience, Abstract, in press) showed increased Molecular and Cellular Mechanisms of Neuronal Plasticity, edited by Ehrlich. Plenum Press. New York, 1998. 2 D. L. Alkon activation of the gene responsible for ryanodine receptor expression after spatial maze learning. Through this molecular cascade, stimuli associated during training increase dendritic excitability and thus increase synaptic weight through enhanced post-synaptic responsive ness, as demonstrated for associative memory within the molluscan (Hermissenda) visual vestibular network. the hippocampus. and the H6 cerebellar cortex. In more recent studies, Calexcitin was found to markedly enhance synaptic EPSP's and to inactivate IPSP's. These mechanisms of memory storage induced in vivo show some convergence with in vi tro models of cellular memory (e.g LTP, LTD, LTT Long-term synaptic transformation-see below) such as involvement of PKC activation. One divergence, however, was confirmed when antisense oligonucleotides to mRNA that codes for mkvl.l in vivo eliminated mem ory retention (Meiri et a!., in press) along with specific voltage-dependent K+ channels, but leaving LTP unimpaired. These conserved molecular and biophysical mechanisms that can regulate synaptic weight during associative memory have also recently been impli cated as targets of pathophysiology induced by nM levels of soluble l3-amyloid in the clinical entity Alzheimer's Disease, recognized by its memory deficits. SYNAPTIC TRANSFORMATIONS DURING ASSOCIATIVE LEARNING In vitro changes of synaptic efficacy in fully differentiated nervous systems have been known and analyzed since Feng first identified post-tetanic potentiation at the neuromuscu lar junction in the late 1930's. Since that time, many additional examples of synaptic effi cacy modification have been identified in diverse species (Katz, 1966; Kuffler et aI., 1984). These include synaptic facilitation at the lobster and crab neuromuscular junctions, hetero synaptic facilitation in the mollusc abdominal ganglion, long-term potentiation (LTP) of glutamatergic EPSP's recorded from pyramidal cells in the rat hippocampus, and long-term depression (LTD) of glutamatergic EPSP's recorded from Purkinje cells of the rat cerebel lum. All of these changes of synaptic efficacy are candidates for synaptic mechanisms pos tulated by such pioneers as Cajal, Sherrington, and Pavlov to provide a physiologic basis for memory. Yet, these examples of synaptic modification have been difficult to observe during associative learning and memory behavior of living animals. To assess in vitro synaptic change(s) in the context of in vivo associative learning and memory, LAS scientists set out many years ago to correlate synaptic changes of effi cacy with behavioral acquisition and retention of associative memory. Pavlovian condi tioning of the mollusc Hermissenda (Alkon, 1983). for example, produced long-term enhancement of type B cell excitability (and thus responsiveness) and thereby enhanced input to and output from downstream motor neurons. Pavlovian conditioning of the rabbit (Thompson. 1986) was shown in LAS studies to enhance post-synaptic dendritic excitabil ity and the amplitude of summated EPSP responses of CA I pyramidal cells (Disterhoft et aI., 1986; Lo Turco et al., \985). Still other LAS studies (Schreurs et al.. 1997) demon strated intradendritic excitability increases in cerebellar microzones after rabbit Pavlovian conditioning (Figure I). All of these examples correlated with and/or could be accounted for by long-term inactivation of voltage-dependent K+ channels (as explained below) and are consistent with current understanding of ion channel distribution within the pyramidal cell dendritic tree (Migliore et a!., 1995). A crucial part of this past research was accom plished when LAS investigators pioneered the analysis of cellular changes within brain slices taken from trained and control animals exposed to a variety of stimulus paradigms.

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