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NEONATAL IBOTENIC ACID LESIONS of the VENTRAL HIPPOCAMPUS: the EFFECTS of STRESS on GENE EXPRESSION and APOPTOSIS a Thesis Submi

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NEONATAL IBOTENIC ACID LESIONS of the VENTRAL HIPPOCAMPUS: the EFFECTS of STRESS on GENE EXPRESSION and APOPTOSIS a Thesis Submi NEONATAL IBOTENIC ACID LESIONS OF THE VENTRAL HIPPOCAMPUS: THE EFFECTS OF STRESS ON GENE EXPRESSION AND APOPTOSIS A thesis submitted to the College of Graduate Studies and Research in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Psychiatry University of Saskatchewan Saskatoon BY Paula C. Ashe Surnmer 2000 O Copyright Paula C. Ashe, 2000. All rights reserved. National Library Bibliothèque nationale du Canada Acquisitions and Acquisitions et Bibliographie Services services bibliographiques 395 WeUington Street 395, rue Weilington OitawaON KlAON4 OuawaON KfAONQ Canada CaMda The author has granted a non- L'auteur a accordé une licence non exclusive licence allowing the exclusive permettant à la National Library of Canada to Bibliothèque nationale du Canada de reproduce, loan, distribute or sell reproduire, prêter, distribuer ou copies of this thesis in microfom, vendre des copies de cette thèse sous paper or electronic formats. la forme de microfiche/film, de reproduction sur papier ou sur format électronique. The author retains ownership of the L'auteur conserve la propriété du copyright in this thesis. Neither the droit d'auteur qui protège cette thèse. thesis nor substantial extracts fiom it Ni la thèse ni des extraits substantiels may be printed or otherwise de celle-ci ne doivent être imprimés reproduced without the author's ou autrement reproduits sans son permission. autorisation. NEONATAL IBOTENIC ACID LESIONS OF THE VENTRAL HIPPOCAMPUS: THE EFFECTS OF STRESS ON GENE EXPRESSION AND APOPTOSIS PAULA C. ASHE PERMISSION TO USE In presenting this thesis in partial fulfillment of the requirements for a Postgraduate degree from the University of Saskatchewan, 1 agree that the Libraries of this University may make it freely available for inspection. 1 further agree that permission for copying of this thesis in any manner, in whole or in part, for scholarly purposes may be granted by the professon who supervised my thesis work, Ors. A.V. Juorio and X.-M. Li or, in their absence, by the Director of the Neuropsychiatry Research Unit or the Head of the Department of Psychiatry. It is understood that any copying or publication or use of this thesis or parts thereof for financial gain shall not be allowed without my written permission. It is also understood that due recognition shall be given to me and to the University of Saskatchewan in any scholarly use which may be made of any material in my thesis. Requests for permission to copy or to make other use of material in this thesis in whole or part should be addressed to: Director of the Neuropsychiatry Research Unit Medical Research Building 103 Wiggins Road University of Saskatchewan Saskatoon, Saskatchewan S7N SE4 Head of the Department of Psychiatry Royal University Hospital Saskatoon, Saskatchewan S7N OWO Recently, it has kensuggested that neurodevelopmental abnormalities underlie schizophrenia. However, it has also been suggested that schizophrenia is a neurodegenerative disease as evidenced by a progressive worsening of symptoms over time. Neurodevelopmental abnormalities may, therefore, create a functionally compromised system that is more susceptible to neuronal atrophy and/or death caused by environmental factors such as stress (a known precipitant of acute psychotic episodes and exacerbant of schizophrenia). This hypothesis was tested using the putative neurodevelopmental animal model of schizophrenia described by Lipska etal: (1993). This model, which parallels a number of aspects of schizophrenia, involves bilateral ibotenic acid lesions in postnatal day 7 male rats. The effects of neonatal hippocampal lesions on BDNF mRNA and NMDARl mRNA, factors involved in development, cell survival and cell communication, were investigated in adult rats following exposure to a physiolog ical stressor. Apoptosis levels were also investigated in these rats to determine if neurodegeneration was present. Results demonstrate that BDNF mRNA was reduced in the prefrontal cortex and hippocampus of lesioned as compared to sham rats. Increased BNDF mRNA resulted from swirn stress in both groups, but the increase in lesioned animals was more pronounced than controls. NMDARl mRNA was also reduced in the prefrontal cortex and CA3 and CA1 regions of the hippocampus in lesioned venus sham rats. There was an increase, however, in the dentate gyrus of lesioned venus sham rats. Swim stress increased NMDARl mRNA in the prefrontal cortex and decreased it in the hippocarnpus. There was also an increase in apoptosis in lesioned versus sham rats, with no significant increase in response to stress. Reductions in BDNF mRNA in lesioned venus control animals support the hypothesis that neurodevelopmental lesions may result in a system more susceptible to stressors. Redudions in NMDARl mRNA are in accordance with the NMDA glutamate receptor hypofundion theory of schizophrenia. It is possible that reductions in glutamate function can remove the inhibitory effed of GABA, thereby resulting in overexcitation of the system and a potential for neurodegeneration. Increased apoptosis supports the presence of neurodegeneration as an ongoing phenornenon, however, it appears that these animals are resistant to increased cell death induced by acute stressors. The question remains whether chronic stress may have more serious consequences in these lesioned animals. iii ACKNOWLEDGEMENTS 1 would like to take this opportunity to extend rny thanks to the people responsible for seeing me through my time as a graduate mident. First, 1 would like to thank my supervisor, Dr. A.V. Juorio and my co-supervisor, Dr. X.- M. Li, for their support and guidance and for the opportunity to develop both scientifically and personaliy. 1 would also like to thank Dr. A.A. Boulton and Dr. R. Bowen for their support, encouragement and helpful suggestions throughout my program. The other members of my committee, Dr. B.A. Davis, Dr. P. Krone and Dr. P.H. Yu, also deserve my greatest thanks for the time they dedicated and the many useful suggestions to aid my research. Many people deserve credit for supporting me and teaching me things along the way. 1 would like to particularly thank Gabriel Stegeman for her unending support, encouragement and help and Edwin Zarycki for starting me off in the right direction. Thanks also go to other students who shared my experiences and to other members of the Neuropsychiatry Unit who never failed to lend a helping hand when it was needed. 1 would also like to extend my sincere thanks to the Schizophrenia Society of Saskatchewan for their tremendous support, both financially and penonally. On a more personal note, the completion of this thesis would not have been possible without the infinite support, encouragement and understanding of rny husband, Lyle, and rny family and friends. To my father, who gave me the strength and determination to face challenges. Thank you. TABLE OF CONTENTS Page PERMISSION TO USE...................................................................................... i .. ABSTRACT........................................................................................................ I I ACKNOWLEDGEMENTS .................................................................................... iv DEDICATION.................................................................................................... v TABLE OF CONTENTS ...................................................................................... vi UST OF TABLES ............................................................................................... x UST OF FIGURES............................................................................................ xi UST OF ABBRMATIONS............................................................................... xiv 1 . INTRODUCnON.................................................................................. 1 1.1 Characteristics of Schizophrenia ....................................................-1 1.2 Neurotransmitter Theories of Schizophrenia.................................. 2 1.2.1 The Dopamine Hypothesis................................................... 3 1.2.2 The Glutamate Hypothesis ........................................................ 4 1.3 Neurodevelopmental Venus Neurodegenerative Theories............ 8 1.3.1 Neuropathological Findings in Schizophrenia ........................... 11 1.3.1.1 Gross Morphological Abnormalities ............................... 11 1.3.1.2 Cytoarchitectonic Abnormalities ..................................... 14 1.3.1.3 Biochemical Abnormalities in Schizophrenia.................. 17 1.3.2 The Dysconnectivity Hypothesis .......................................... 23 1.4 A Neurodevelopmenlal Animal Model of Schizophrenia................ 25 1.4.1 Characteristics of the Model...................................................... 25 1.4.2 Parallels to Schizophrenia ......................................................... 29 1.4.3 Implications and Limitations of the Model ................................ 33 1.5 Potential Factors Involved in Schizophrenia.................................. 34 1.5.1 Stress ......................................................................................... 34 1S.2 Brain-Derived Neurotrophic Factor ........................................... 37 1.5.3 N-Methyl-o-Aspartate Glutamate Receptor............................... 40 1S.4 Apoptosis ................................................................................... 41 1.6 Objectives of the Project.
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