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<p>Episodic memory formation is shaped by expectation. Events that generate expectations have the capacity to influence memory. Additionally, whether subsequent events meet or violate expectations has consequences for memory. However, clarification is still required to illuminate the circumstances and direction of memory modulation. In the brain, the mechanisms by which expectation modulates memory formation also require consideration. The dopamine system has been implicated in signaling events associated with different states of expectancy; it has also been shown to modulate episodic memory formation in the hippocampus. Thus, the studies included in this dissertation utilized both functional magnetic resonance imaging (fMRI) and behavioral testing to examine when and how the dopaminergic system supports the modulation of memory by expectation. The work aimed to characterize the activation of dopaminergic circuitry in response to cues that generate expectancy, during periods of anticipation, and in response to outcomes that resolve expectancy. The studies also examined how each of these event types influenced episodic memory formation. The present findings demonstrated that novelty and expectancy violation both drive dopaminergic circuitry capable of contributing to memory formation. Consistent with elevated dopaminergic midbrain and hippocampus activation for each, expected versus expectancy violating novelty did not differentially affect memory success. We also showed that high curiosity expectancy states drive memory formation. This was supported by activation in dopaminergic circuitry that was greater for subsequently remembered information only in the high curiosity state. Finally, we showed that cues that generate high expected reward value versus high reward uncertainty differentially modulate memory formation during reward anticipation. This behavioral result was consistent with distinct temporal profiles of dopaminergic action having differential downstream effects on episodic memory formation. Integrating the present studies with previous research suggests that dopaminergic circuitry signals events that are unpredicted, whether cuing or resolving expectations. It also suggests that contextual differences change the contribution of the dopaminergic system during anticipation, depending on the nature of the expectation. And finally, this work is consistent with a model in which dopamine elevation in response to expectancy events positively modulates episodic memory formation.</p> / Dissertation

A thesis submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg, for the degree of Doctor of Philosophy (Medicine) / Idiopathic Parkinson's disease remains one of the commonest neurodegenerative diseases known today. It causes incapacita ting symptoms untreated but when given replacement neurotransmitters, principally levodopa or dopamine, corrects the major features of the illness. The fundamental cause of nigral dopaminergic cell decline remains unknown, is not principally genetic, but may be due to abnormal hepatic handling of neurotoxins. One such putative neurotovin is MPTP which causes parkinsonism in man and primates. The MPTP-treated primate model is thus a useful model within which new drugs, including dopamine receptor agonists may be tested. Levodopa remains the mainstay of successful pharmacotherapy in the treatment of parkinson's disease. However the last decades have taught us that levodopa treatment with time produces problems of dyskinesias and unpredictable motor fluctuations. Hence alternate pharmacotherapy is sought to supplement levodopa or possibly to circumvent its necessity. (Abbreviation abstract) / Andrew Chakane 2019

Wong Kwok Kui Wister. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 220-236). / ABSTRACT --- p.1 / OBJECTIVES FOR PROJECT --- p.4 / ABBREVIATIONS --- p.6 / Chapter CHAPTER 1 --- INTRODUCTORY LITERATURE REVIEWS / Chapter 1.1 --- Noradrenaline and adrenaline / Chapter 1.1.1 --- History --- p.8 / Chapter 1.2 --- The adrenal medulla / Chapter 1.2.1 --- The anatomy and microcirculation of the adrenal medulla --- p.10 / Chapter 1.2.2 --- Neuro-endocrine control of adrenal medullary secretion --- p.12 / Chapter 1.3 --- Dopamine / Chapter 1.3.1 --- Introduction --- p.14 / Chapter 1.3.2 --- Levels of DA in plasma and urine --- p.14 / Chapter 1.3.3 --- Origins of DA in the urine --- p.15 / Chapter 1.3.4 --- Control of renal DA production --- p.16 / Chapter 1.3.5 --- The actions of DA in the body --- p.17 / Chapter 1.3.6 --- The DA hypothesis --- p.17 / Chapter 1.3.7 --- Urinary NA and AD --- p.18 / Chapter 1.4 --- ACE inhibitors / Chapter 1.4.1 --- Brief review of the pharmacology of ACE inhibitors --- p.19 / Chapter 1.5 --- Catecholamine assays / Chapter 1.5.1 --- Introduction --- p.21 / Chapter 1.5.2 --- Chemistry --- p.22 / Chapter 1.5.3 --- Bioassay --- p.23 / Chapter 1.5.4 --- Colorimetry --- p.25 / Chapter 1.5.5 --- Fluorometry --- p.25 / Chapter 1.5.6 --- Radiochemical techniques --- p.27 / Chapter 1.5.7 --- Radioimmunoassay --- p.29 / Chapter 1.5.8 --- Chromatography --- p.30 / Chapter CHAPTER 2 --- METHODS - DEVELOPMENT OF A CATECHOLAMINE ASSAY & STABILITY STUDIES ON CATECHOLAMINES / Chapter 2.1 --- High performance liquid chromatography and electrochemical detection of catecholamines / Chapter 2.1.1 --- Introduction --- p.38 / Chapter 2.1.2 --- Basic equipment --- p.39 / Chapter 2.1.3 --- Stock aqueous CAT standards --- p.40 / Chapter 2.1.4 --- Mobile phase of HPLC-ECD --- p.40 / Chapter 2.1.5 --- Determination of mobile phase composition and flow rate --- p.41 / Chapter 2.1.6 --- Electrochemical detection --- p.43 / Chapter 2.1.7 --- Linearity and lowest detection limit of HPLC-ECD system --- p.49 / Chapter 2.1.8 --- Maintenance of HPLC-ECD system --- p.54 / Chapter 2.1.9 --- Discussion --- p.56 / Chapter 2.2 --- Sample pre-treatment & stability studies - Human urine / Chapter 2.2.1 --- Pre-treatment --- p.58 / Chapter 2.2.2 --- Analytical performance of the assay --- p.63 / Chapter 2.2.3 --- Stability studies --- p.85 / Chapter 2.2.4 --- Discussion --- p.101 / Chapter 2.2.5 --- Conclusions --- p.108 / Chapter 2.3 --- Sample pre-treatment & stability studies - Rat urine / Chapter 2.3.1 --- Pre-treatment --- p.111 / Chapter 2.3.2 --- Analytical performance of the assay --- p.111 / Chapter 2.3.3 --- Stability studies --- p.119 / Chapter 2.3.4 --- Discussion --- p.131 / Chapter 2.3.5 --- Conclusions --- p.133 / Chapter CHAPTER 3 --- "URINARY CREATININE, SODIUM AND POTASSIUM MEASUREMENTS" / Chapter 3.1 --- Introduction --- p.135 / Chapter 3.2 --- Method / Chapter 3.2.1 --- Urinary creatinine measurement --- p.135 / Chapter 3.2.2 --- Urinary sodium and potassium measurement --- p.136 / Chapter 3.3 --- Results / Chapter 3.3.1 --- Urinary creatinine measurement --- p.136 / Chapter 3.3.2 --- Urinary sodium and potassium measurement --- p.136 / Chapter 3.4 --- Discussion / Chapter 3.4.1 --- Urinary creatinine measurement --- p.136 / Chapter 3.4.2 --- Urinary sodium and potassium measurement --- p.137 / Chapter 3.5 --- Statistics --- p.138 / Chapter 3.6 --- Chemicals --- p.139 / Chapter CHAPTER 4 --- STUDIES ON URINARY EXCRETION OF CATECHOLAMINES IN MAN / Chapter 4.1 --- Population study on the relationships between dietary salt intake and urinary catecholamine output / Chapter 4.1.1 --- Introduction --- p.141 / Chapter 4.1.2 --- Method --- p.142 / Chapter 4.1.3 --- Results --- p.143 / Chapter 4.1.4 --- Discussion --- p.148 / Chapter 4.1.5 --- Conclusions --- p.149 / Chapter 4.2 --- The effect of oral salt loading on urinary catecholamine output / Chapter 4.2.1 --- Introduction --- p.149 / Chapter 4.2.2 --- Methods --- p.150 / Chapter 4.2.3 --- Results --- p.152 / Chapter 4.2.4 --- Discussion --- p.159 / Chapter 4.2.5 --- Conclusions --- p.161 / Chapter 4.3 --- The effects of perindopril on urinary catecholamine outputs / Chapter 4.3.1 --- Introduction --- p.162 / Chapter 4.3.2 --- Methods --- p.165 / Chapter 4.3.3 --- Results --- p.166 / Chapter 4.3.4 --- Discussion --- p.189 / Chapter 4.3.5 --- Conclusions --- p.190 / Chapter CHAPTER 5 --- STUDY ON URINARY EXCRETION OF CATECHOLAMINES AFTER ORAL ADMINISTRATION OF CAPTOPRIL TO RATS / Chapter 5.1 --- Introduction --- p.192 / Chapter 5.2 --- Methods --- p.192 / Chapter 5.3 --- Results --- p.193 / Chapter 5.4 --- Discussion --- p.210 / Chapter 5.5 --- Conclusions --- p.212 / Chapter CHAPTER 6 --- CONCLUSIONS --- p.214 / Chapter CHAPTER 7 --- FUTURE PROSPECTS --- p.216 / PUBLICATIONS TO DATE --- p.218 / ACKNOWLEDGEMENTS --- p.219 / REFERENCES --- p.220

by Ho, Chung Shun. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves [304-328]). / Chapter CHAPTER 1 --- REVIEW ON SODIUM EXCRETION / Chapter L --- Sodium excretion --- p.1-1 / Chapter II. --- Cellular mechanism of sodium reabsorption --- p.1-3 / Chapter III. --- Sensors monitoring ECF volume --- p.1-6 / Chapter IV. --- Factors affecting natriuresis: / Glomerular filtration rate --- p.1-8 / Renal physical forces --- p.1-8 / Sympathetic nervous system --- p.1-10 / Renal dopamine --- p.1-12 / Renin-angiotensin system --- p.1-14 / Aldosterone --- p.1-16 / Renal prostaglandins --- p.1-17 / Renal kallikrein-kinin system --- p.1-18 / Natriuretic peptides --- p.1-19 / Endogenous sodium transport inhibitor --- p.1-21 / Vasopressin --- p.1-22 / Endothelins --- p.1-23 / Endothelin-derived relaxing factor --- p.1-25 / Other hormones --- p.1-25 / Chapter V. --- Conclusion --- p.1-27 / Chapter CHAPTER 2 --- MEASUREMENT OF ENDOGENOUS SODIUM TRANSPORT INHIBITORS / Chapter I. --- Literature review: --- p.2-1 / Pretreatment and purification procedures prior to ESTI measurement --- p.2-1 / Methods of measuring ESTI --- p.2-3 / "Inhibition of purified Na, K-ATPase activity" / Inhibition of sodium pump on intact cells or tissues / Biological effects of sodium pump inhibition / Immunoreactivity with anti-digoxin /anti-ouabain antibodies / Chapter II. --- Method of measurement of ESTI in this study: / Principles of methods --- p.2-11 / Materials and methods --- p.2-14 / Results --- p.2-24 / Discussion --- p.2-53 / Chapter CHAPTER 3 --- MEASUREMENT OF URINARY FREE DOPAMINE / Chapter I. --- Literature review / Properties of dopamine for measurement methods --- p.3-1 / Preservatives used in the urine collection --- p.3-3 / Sample pretreatment procedure before --- p.3-6 / measurement --- p.3-8 / Methods of measurement / Bioassays / Colorimetric method / Fluorometric methods / Radioimmunoassays / Radioenzymatic method / Chromatographic methods --- p.3-16 / Concluding remarks / Chapter II. --- Method of measurement in this study / Principle of the method --- p.3-17 / Materials and methods --- p.3-18 / Results --- p.3-23 / Discussion --- p.3-54 / Chapter CHAPTER 4 --- CROSS SECTIONAL STUDIES IN THE HUMAN / Chapter I. --- Introduction --- p.4-1 / Chapter II. --- Relationship of urinary sodium excretion and plasma ESTI in medical students / Materials and methods --- p.4-2 / Results --- p.4-3 / Discussion --- p.4-6 / Chapter III. --- Excretion of urinary electrolytes and natriuretic factors in young Chinese females / Materials and methods --- p.4-7 / Results --- p.4-8 / Discussion --- p.4-11 / Chapter IV. --- Urinary sodium / DA relationship in Chinese normotensives and hypertensives --- p.4-13 / Materials and methods / Results --- p.4-14 / Discussion --- p.4-17 / Chapter V. --- Urinary DA excretion and plasma ESTI in normotensive and hypertensive NIDDM patients / Materials and methods --- p.4-20 / Results --- p.4-23 / Discussion --- p.4-33 / Chapter CHAPTER 5 --- VOLUME EXPANSION STUDIES IN THE HUMAN / Chapter I --- Introduction --- p.5-1 / Chapter II. --- Volume expansion by headout water immersion / Materials and methods --- p.5-3 / Results --- p.5-5 / Discussion --- p.5-11 / Chapter III. --- Volume expansion by saline infusion / Materials and methods --- p.5-16 / Results --- p.5-19 / Discussion --- p.5-29 / Chapter IV. --- Oral salt loading with free diet / Materials and methods --- p.5-36 / Results --- p.5-38 / Discussion --- p.5-49 / Chapter V. --- Oral salt loading under controlled diet / Materials and methods --- p.5-53 / Results --- p.5-54 / Discussion --- p.5-64 / Chapter CHAPTER 6 --- STUDIES ON THE EFFECTS OF SALT LOADING IN THE RAT / Chapter I. --- Introduction --- p.6-1 / Chapter II. --- Temporal relationship between excretions of DA and ESTI during salt loading in the rat / Materials and methods --- p.6-2 / Results --- p.6-3 / Discussion --- p.6-6 / Chapter III. --- Roles of DA and ESTI in natriuresis in rats treated with carbidopa / Materials and methods --- p.6-8 / Results --- p.6-9 / Discussion --- p.6-14 / Chapter CHAPTER 7 --- CONCLUSION / Measurement of ESTI --- p.7-2 / Measurement of urinary free DA --- p.7-5 / Cross sectional studies in human --- p.7-7 / Volume expansion studies in human --- p.7-11 / Studies on the effects of salt loading in the rat --- p.7-16 / Summary --- p.7-18

ix, 237 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D. 1979) from the Dept. of Obstetrics and Gynaecology, University of Adelaide