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Global Reactivation and Targeted Preservation of Mecp2 Expression in a Mouse Model of Rett Syndrome

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Global Reactivation and Targeted Preservation of Mecp2 Expression in a Mouse Model of Rett Syndrome Global Reactivation and Targeted Preservation of MeCP2 Expression in a Mouse Model of Rett Syndrome By Min Lang A thesis submitted in conformity with the requirements for the degree of Master of Science Graduate Department of Physiology University of Toronto I Ubiquitous Reactivation and Targeted Preservation of MeCP2 Expression in a Mouse Model of Rett Syndrome Min Lang Master of Science, 2012 Department of Physiology University of Toronto Abstract Rett syndrome is a neurodevelopmental disorder that is predominately caused by mutations of the MECP2 gene. As neuronal apoptosis is not observed in RTT patients and MeCP2-deficient mice, the neurological deficits may be reversible. To address this, we reactivated MeCP2 expression ubiquitously in MeCP2-deficient mice after symptom onset. Our results showed that life span, behavioural performances, EEG activity, thermoregulation, and daily rhythmic activity were significantly improved after MeCP2 reactivation. Furthermore, the extent of improvement was dependent upon the efficiency of MeCP2 reactivation. To assess the role of the catecholaminergic system in Rett syndrome pathophysiology, we selectively preserved MeCP2 function within tyrosine hydroxylase expressing cells. We observed a significant improvement in the life span of male rescue mice and reduced sudden unexplained death rates in female rescue mice. Behavioural performances and EEG patterns were also significantly improved. II Acknowledgements I would like to thank Dr. Eubanks for giving me the opportunity to pursue research in his lab and taking the time to teach me and guide me throughout my Master’s project. Dr. Zhang for teaching me about the field of EEG and guiding me through my projects. Chiping Wu for implanting all of the mice that was used for the studies. Richard Logan and Guanming Zhang for teaching me laboratory techniques that was used for my research. Dr. Hampson and Dr. Mount for their guidance and advice throughout my project. Elena Sidorova, Natalya Shulyakova, and Robert Wither for their help, advice, and support during my Master’s. III Table of Contents Title Page ............................................................................................................................. I Abstract ............................................................................................................................... II Acknowledgements ............................................................................................................III Table of Contents .............................................................................................................. IV List of Figures ................................................................................................................... IX 1. Introduction ....................................................................................................................1 1.1. General Overview (RTT) ..............................................................................................1 1.2. Clinical features of Rett syndrome ...............................................................................2 1.3. Pathophysiology of Rett syndrome ...............................................................................6 1.3.1. Neuropathology......................................................................................................6 1.3.2. Neurochemistry ......................................................................................................7 1.4. Electroencephalogram abnormalities and epileptic seizures ........................................8 1.5. Autonomic deficits ........................................................................................................9 1.6. Rett syndrome and MECP2 ........................................................................................10 1.7. MeCP2 function ..........................................................................................................11 1.8. Mouse models of Rett syndrome ................................................................................15 1.9. Gross phenotypes of Rett syndrome mouse models ...................................................21 1.10. Targeted deletion of MeCP2 expression ...................................................................22 1.11. Reversibility of deficits in mouse models of Rett syndrome ....................................26 1.12. Gene therapy .............................................................................................................28 IV 1.13. Pharmacological treatments ......................................................................................28 1.14. Rationale and hypothesis ..........................................................................................31 1.14.1. Project1: Delayed ubiquitous reactivation of MeCP2 .......................................31 1.14.2. Project 2: Preservation of MeCP2 function in catecholaminergic cells ............33 1.15. Project aims ...............................................................................................................35 2. Materials and Methods ................................................................................................38 2.1. Mice ............................................................................................................................38 2.2. Western blotting ..........................................................................................................39 2.3. Immunohistochemistry ...............................................................................................40 2.4. Tamoxifen treatment ...................................................................................................40 2.5. Electrophysiology data collection ...............................................................................41 2.6. Behavioural assessments .............................................................................................41 2.7. Phenotypic severity scoring ........................................................................................42 2.8. Cell counting ...............................................................................................................43 2.9. Telemetry probe implantation protocol ......................................................................43 2.10. Tethered electrode implantation ...............................................................................44 2.11. Electroencephalographic recordings and analysis ....................................................44 2.12. Statistics ....................................................................................................................45 3. Results ...........................................................................................................................46 3.1.1 Rescue of MeCP2 expression in Stop/y,cre mice .....................................................46 3.1.2. Restoration of MeCP2 rescues life span and gross phenotypic severity .................49 3.1.3. Extent of behavioral rescue is dependent upon MeCP2 reactivation percentage ....52 3.1.4. Epileptiform discharges are significantly attenuated after MeCP2 reactivation .....57 V 3.1.5. Reactivation of MeCP2 in female MeCP2-deificient mice rescues behavioral performances ......................................................................................................................60 3.1.6. MeCP2 reactivation improves daily rhythmic activity and thermoregulation in adult female MeCP2-deficient mice ...........................................................................................63 3.2.1. MeCP2 is selectively preserved in tyrosine hydroxylase-expressing neurons in the “Rescue” mouse brain ........................................................................................................71 3.2.2. Preservation of MeCP2 in catecholaminergic cells extends the lifespan of male MeCP2-deficient mice .......................................................................................................77 3.2.3. Preservation of MeCP2 in catecholaminergic cells decreases the rate of sudden unexpected death in female MeCP2-deficient mice ..........................................................80 3.2.4. Catecholaminergic preservation of MeCP2 improves deficits in ambulatory rate, motor coordination, and anxiety-like behavior in male MeCP2-deficient mice ................83 3.2.5. Catecholaminergic preservation of MeCP2 improves the ambulatory and anxiety-like behavioral deficits of adult female MeCP2-deficient mice ...............................................86 3.2.6. Preservation of MeCP2 in catecholaminergic cells improves cortical EEG abnormalities in male, but not female, MeCP2-deficient mice .........................................90 3.2.7. Preservation of MeCP2 in catecholaminergic cells improves peak hippocampal theta frequency in male, but not female, MeCP2-deficient mice ...............................................96 3.2.8. Preservation of MeCP2 in catecholaminergic cells rescues deficits in hippocampal gamma band oscillatory activity in male, but not female, MeCP2-deficient mice ..........100 4. Discussion....................................................................................................................105 4.1. Part 1: Delayed global reactivation of MeCP2 expression .......................................105 4.2. Part 2: Selective preservation of MeCP2 functions in catecholaminergic
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